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THE  LIBRARY 

OF 

THE  UNIVERSITY 

OF  CALIFORNIA 

LOS  ANGELES 

GIFT  OF 
Mrs.  Clifford  B.  Walker 


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LECTURES 


ON 


THE    HUMAN    EYE 


IN    ITS 


NORMAL  AND  PATHOLOGICAL  CONDITIONS 


BY 

ADOLF   ALT,  M.  D. 

Lecturer  on    Ophthalmology    and   Otology   in    the   Trinity    Medical  School 
Toronto,  Canada 


WITH  95  ILLUSTRATIONS  BY  THE  AUTHOR 


NEW   YORK 

G.  P.  P  U  T  N  A  M  •  S  S  O  N  S 

182  Fifth  Avenue 

1880. 


Coi'VRjGHT,  1880,  Bv  G.  P.  Putnam's  Sons,  New  York. 


Biomedical 
Library 

WvV 
lot 


DEDICATION. 


THIS   BOOK    IS   DEDICATED    TO    THE    MEMORY    OF    MY    FATHER, 

DETTMAR  ALT, 

LATE    PHYSICIAN    IN     MANNHEIM,    AND     HIS    FRIENDS,    MY    HIGHLY- 
ESTEEMED    TEACHERS, 

DR.  TH.  VON  DUSCH, 

PROFESSOR    AT    HEIDELBERG,    AND 

DR.  H.  KNAPP, 

OF    NEW    YORK,    FORMERLY    PROFESSOR    AT    HEIDELBERG. 


635920 


PREFACE. 


The  histological  conditions  of  the  human  eye  have 
of  late  received  a  good  deal  of  attention,  and  their 
study  has  been  opened  to  a  wider  circle  by  a  number 
of  atlases, -which,  like  the  one  published  conjointly  by 
Pagenstecher  &  Genih,  and  another  by  Becker^  can 
boast  of  an  excellent  execution. 

A  book  treating  systematically  on  this  subject, 
and  especially  on  the  histological  conditions  of  the 
pathological  human  eye,  whose  execution  and  price 
would  allow  it  to  be  of  usefulness  to  every  one  in- 
terested in  this  matter,  has  been  to  this  day  a  want 
often  felt. 

For  quite  a  number  of  years  I  have  been  engaged 
in  collecting  for  my  own  instruction,  microscopical 
specimens  of  normal  and  pathological  eyes.  This 
material  for  examination,  especially  its  pathological 
part,  has  by  the  kindness  of  Dr.  H.  Knapp,  of  New 
York,  and  a  great  many  other  colleagues,  to  whom 
my  sincerest  thanks  are  due,  become  so  large,  that  I 
think  it  in  season  to  give  the  results  of  my  researches 
to  the  medical  public  in  systematic  order.  I  have 
confined  myself,  however,  in  this  book  entirely  to 
the  eye-ball  itself,  and  have  left  the  accessory  parts 
to  be  treated  at  a  later  period,  when  I  shall  be 
better  able  to  do  so  than  I  can  at  present,  on  ac- 
count of  the  scarcity  of  material  which  is  at  my 
disposal.  Furthermore,  I  have  given  especial  atten- 
tion to  the  pathological  conditions  of  the  eye-ball. 
This  I  thought  only  natural,  as  with   regard   to  the 


Vi  PREFACE. 

normal  conditions  I  could  bring  forward  but  little 
that  was  new ;  and  I  could  doubtlessly  presume  that 
all  my  readers  would  be  more  or  less  acquainted 
with  these. 

All  of  the  illustrations  are  drawn  from  my  own 
specimens,  and  I  have  anxiously  tried  to  copy  only 
what  I  really  saw  without  being  influenced  by  pre- 
conceived ideas. 

I  have  thought  it  unnecessary  to  enlarge  the  book 
by  an  elaborate  record  of  all  the  authors  and  articles 
I  consulted,  when  studying  up  this  subject,  as  a  sum- 
mary of  them  may  be  found  in  Graefe  &  Saemisch's 
cyclopedia.  I  have  endeavored,  however,  to  do  jus- 
tice to  every  author  whose  opinion  I  stated,  confirmed, 
or  disagreed  with,  by  adding  the  name  in  brackets.  If 
in  consequence  of  having  only  my  own  comparatively 
small  library  at  my  disposal,  I  should  have  unconsci- 
ously omitted  some,  or  been  mistaken  with  regard  to 
others,  I  beg  herewith  the  pardon  of  the  persons  of- 
fended. Since  the  German  manuscript,  of  which  this 
book  is  a  translation,  was  finished  during  November, 
1878,  of  course  I  could  not  take  into  account  the  lit- 
erature of  this  year. 

This  book  is  an  elaboration  of  the  notes  written 
down  while  lecturing  on  the  subject  under  consid- 
eration, at  the  New  York  Ophthalmic  and  Aural 
Institute  in  1876  and  1877.  Since  these  lectures 
were  kindly  and  forbearingly  received  by  my  audi- 
ence, I  may,  perhaps,  venture  to  hope  that  they  will 
also  find  readers  who  will  peruse  them  in  the  same 
spirit.  And  if  this  book  should  be  able  to  en- 
large the  interest  already  taken  in  the  study  of  the 
histology  of  the  finest  human  organ,  and  to  act  as  a 
new  stimulus  to  renewed  strife  to  fill   up  the  chasms 


PREFACE. 


yet  unfilled  in  our  knowledge,   what  labor   I   had  to 
bestow  on  it  will  be  amply  repaid. 

My  sincerest  thanks  are  due  to  Dr.  T.  R.  Pooley, 
of  New  York,  who  has  kindly  undertaken  the  revision 
of  the  manuscript  and  proofs  of  my  volume  with  a  view 
to  the  correction,  as  far  as  practicable,  of  any  errors 
of  style  or  expression. 

The  Author. 

Toronto,  Canada,  August,  1879. 


CONTENTS. 


PAGE 

Preface i 

I.  Cornea. 

1.  Normal  conditions I 

2.  Pathological  conditions 1 1 

A .  Keratitis  and  its  results 1 1 

a.  Infiltration  of  the  cornea I3 

b.  Purulent  Keratitis i6 

0.  Abscess  of  the  cornea i6 

y3.  Ulcer  of  the  cornea 19 

y.  Keratomalacia 22 

The  Results  of  Keratitis. 

a.  Formation  of  scars  and  pannus 23 

3.  Anterior  synechias 25 

c.  Prolapsus  iridis  and  granuloma  iridis  traumaticum 29 

d.  Keratoconus  e  cicatrice  and  staphyloma  cornese 29 

e.  Pterygiam 30 

B.  Injuries  of  the  cornea,  their  mode  of  healing  and  results 31 

a.  Injuries  without  retention  of  a  foreign  body 31 

b.  Wounds  with  retention  of  a  foreign  body 36 

c.  Burns  with  lime 37 

C.  Regressive  metamorphoses 3S 

D.  Tumors  of  the  cornea 3S 

II.  Sclerotic. 

1.  Normal  conditions 39 

2.  Pathological  conditions 42 

A.  Sclerilis  and  its  results 42 

a.  Infiltration-scleritis 42 

b.  Purulent  scleritis 43 

The  Results  of  Scleritis. 

a.  Formation  of  scars 44 

b.  Prolapse   and   incarceration  of  iris,   ciliary  body,  choroid,   retina, 

crystalline  lens  and  vitreous  body  in  the  sclerotic 45 

c.  Hypertrophy  of  the  sclerotic 45 

d.  Atrophy  of  the  sclerotic  and  ectasy  (staphyloma  of  the  sclerotic). .  46 

1.  The  anterior  staphyloma  of  the  sclerotic 47 

0.  The  corneo-scleral  staphyloma 47 

/?.  The  ciliary  staphyloma 48 

2.  The  equatorial  staphyloma  of  the  sclerotic 49 

3.  The  posterior  staphyloma  of  the  sclerotic 49 


X  CONTENTS. 

PAGE 

B.  Injuries  to  the  sclerotic  and  their  results 51 

a.  Wounds  without  subsequent  retention  of  a  foreign  body 51 

b.  Wounds  with  subsequent  retention  of  a  foreign  body 53 

C.  Tumors  of  the  sclerotic 54 

III.  Conjunctiva  Bulbi  and  the  Episcleral  Tissue. 

1.  Normal  conditions 55 

2.  Pathological  conditions 57 

A.  Conjunctivitis  and  its  results 58 

a.  Conjunctivitis  catarrhalis,  episcleritis,  phlyctaenula 58 

b.  Conjunctivitis  blennorrhoica  (purulenta,  gonorrhoica),  ulcer  of  the 

conjunctiva 59 

c.  Conjunctivitis  crouposa  and  diphtheritica 61 

d.  Conjunctivitis  trachomatosa 61 

The  Results  of  Conjunctivitis. 

B.  Injuries  to  the  conjunctiva  and  their  results 63 

1.  Wounds  without  retention  of  a  foreign  body 63 

2.  Wounds  with  subsequent  retention  of  a  foreign  body 64 

3.  Bums  with  lime - 64 

C.  Tumors  of  the  conjunctiva  bulbi  and  episcleral  tissue 65 

a.  Lymphangiectasia  and  serous  cysts 65 

b.  Granuloma  (polypus) 66 

c.  Dermoid  and  lipomatous  tumors 67 

d.  Fibroma  and  osteoma 69 

e.  Papilloma,  melanoma  and  melanocancroid  new-formations 69 

f.  Leucosarcoma  and  melanosarcoma 71 

g.  Epithelioma 74 

IV.  Iris. 

r.  Normal  conditions 81 

2.  Pathological  conditions 84 

A.  Iritis  and  its  results 84 

a.  Iritis  serosa  (sero-fibrinosa,  haemorrhagica) 8.1 

b.  Iritis  fibrinosa  (plastica) 87 

c.  Iritis  purulenta  (parenchymatosa) 89 

The  Results  of  Iritis. 

a.  Synechise  of  the  iris 91 

b.  Atrophy  of  the  iris 92 

B.  Injuries  to  the  iris  and  their  results '. 93 

C.  Tumors  of  the  iris 97 

a.  Granuloma  traumaticum 97 

b.  Melanoma 97 

c.  Leucosarcoma  and  melanosarcoma 98 

V.  Corpus  cimare. 

1.  Normal  conditions 99 

2.  Pathological  conditions 103 

A.  Cycliiis  and  its  results 103 


CONTENTS.  xi 

PAGK 

a.  Cyclitis  serosa , 103 

b.  Cyclitis  fibrinosa  (plastica) 105 

c.  Cyclitis  purulenta  (parenchymntosa) 109 

The  Results  of  Cyclitis. 

a.  Cyclitic  membranes iii 

b.  Atrophy 113 

c.  Staphyloma 113 

B.  Injuries  to  the  ciliary  body  and  their  results 113 

C.  Tumors  of  the  ciliary  body 115 

a.  Myoma 115 

b.  Sarcoma 115 

VI.  Choroidea. 

1.  Normal  conditions 116 

2.  Pathological  conditions 120 

A.  Pathological  changes  of  the  pigmented  epithelium 120 

B.  Choroiditis  and  its  results 125 

a.  Choroiditis  serosa  (sero-fibrinosa) 125 

b.  Choroiditis  fibrinosa  (plastica) 127 

c.  Choroiditis  purulenta  (parenchymatosa). ...    % 130 

The  Results  of  Choroiditis. 

a.  Detachment  of  the  retina  and  vitreous  body 133 

b.  I^iquefaction  of  the  vitreous  body 134 

c.  Glaucomatous  excavation  of  the  optic  papilla 134 

d.  Atrophy  ;  synechia  between  retina  and  choroid,  and  pigmentation 

of  the  former 134 

e.  Ossification 135 

/.  Staphyloma 136 

C.  Injuries  to  the  choroid  and  their  results 136 

D.  Tumors  of  the  choroid 138 

a.  Cystoid  formations 138 

b.  Granuloma 138 

c.  Sarcoma 138 

VII.  Opticus. 

1.  Normal  conditions 142 

2.  Pathological  conditions 146 

a.  CEdema  of  the  optic  nerve  and  papilla 147 

b.  Vaginitis  nervi  optici 149 

c.  Neuritis  interstitialis  nervi  optici 150 

d.  Neuritis  medullans  nervi  optici 152 

Results  of  the  affections  detailed  in  the  foregoing 153 

Glaucomatous  atrophy  and  excavation,  and  atrophy  of  the  optic 
nerve  caused  by  embolism 155 

Hzemorrhages  in  the  ocular  part  of  the  optic  nerve  and  hsematogene- 
ous  pigmentation 156 

Tumors  of  the  ocular  part  of  the  optic  nerve 157 


xii  CONTENTS. 

PAGE 

VIII.  Retina. 

1.  Normal  conditions 159 

2.  Pathological  conditions i68 

A.  CEdema  of  the  retina i68 

B.  Inflammatory  processes  in  the  retina  and  their  results  169 

a.  Retinitis  albuminurica     169 

b.  Retinitis  interstitialis  diffusa  (atrophica) 174 

c.  Retinitis  purulenta 177 

C.  Changes  in  the  structure  of  the  retinal  blood-vessels,  haemorrhages 

and  detachment  of  the  retina    1 78 

The  Results  of  Retinitis. 

D.  Injuries  to  the  retina  and  their  results ,00 182 

E.  Tumors  of  the  retina 183 

a.  Fibroma 183 

b.  Small-celled  medullary  sarcoma  (glioma) 183 

IX.  Lens  Crystai.linea. 

r.  Normal  conditions 187 

2.  Pathological  conditions 190 

A.  Cataracts  formed  within  an  intact  lens-capsule 190 

B.  Injuries  to  the  lens-capsule  and  lens-substance,  and  their  results. .  194 

X.  Vitreous  Body  and  Zonula  Zinnii. 

1.  Normal  conditions  of  the  vitreous  body 198 

2.  Pathological  conditions  of  the  vitreous  body 199 

A.  Liquefaction  of  the  vitreous  body  (synchisis) 200 

B.  Plastic  hyalitis 201 

C.  Purulent  hyalitis 202 

Zonula  Zinnii. 

1.  Normal  conditions 203 

2.  Pathological  conditions 204 


ILLUSTRATIONS. 


PAGE 

Fig.  I.  (i)  The  interfibrillar  canals.     (2)  Interlamellar  canals  and  lacunoe. 

N.  Nerve-sheath  filled  with  the  injection-fluid 5 

Fig.  2.  Corneo-scleral  margin.  C.  Cornea.  S.  Sclerotic.  CS.  Schlemm's 
canal.  D.  Descemetic  mcmljrane.  I.  Iris.  Lp.  The  fibres  of  the  liga- 
mentum  pectinatum  with  endothelial  cells  adhering  to  them 8 

Fig.  3.  Isolated  fibres  of  the  ligamentum  pectinatum.     The  endothelial  cells 

are  shrunken  and  appear  as  darker  swellings 9 

Fig.  4.  Cavity  of  an  abscess  in  the  cornea,  after  the  contents  have  become 

absorbed 18 

Fig.  5.  Proliferation  of  the  endothelium  of  Descemet's  membrane,  observed 

in  a  case  of  corneal  abscess  with  hypopyon iS 

Fig.  6.  Ulcer  of  the  cornea;  its  ground  and  walls  filled  with  round-cells, 

the  surrounding  epithelium  proliferating 19 

Fig.  7.   Healed  corneal  ulcer.     The  loss  of  substance  filled  with  new-formed 

connective-tissue  into  which  tlie  epithelial  layer  sends  papillary  offsets.      21 

Fig.  8.  Deposits  of  lime  in  the  cornea  of  a  staphylomatous  eye 24 

Fig.  9.  Anterior  .synechia  between  cornea  and  iris.  The  endothelium  of 
Descemet's  membrane  forming  a  layer  of  spindle-shaped  cells  around 
the  place  where  iris  and  cornea  are  united 26 

Fig.  10.  Anterior  synechia  l:)etween  cornea  and  vitreous  body 28 

Fig.  II.  Staphyloma  of  the  cornea,  with  hypertrophy  of  the  latter 30 

Fig.  12.  Section  through  a  pterygium  in  a  meridional  direction.  Pi.  Ptery- 
gium. A.  Corneal  lamellae  raised  by  the  pterygium.  B.  Bowman's 
layer.     C.  Normal  corneal  lamellae 31 

Fig.  13.  Equatorial  section  through  a  pterygium.  Pt.  Pterygium.  S.  Scler- 
otic (corneo-scleral  margin).  E.  Encapsuled  conjunctival  epithelium, 
undergoing  regressive  metamorphoses 32 

Fig.  14.  A  healing  corneal  wound  four  days  after  it  was  inflicted 33 

Fig.  15.  Showing  how  the  stump  of  the  iris  may  be  caught  in  the  corneal 

wound  after  iridectomy 35 

Fig.  16.  Pigmented  cystoid  formation  in  the  cornea 36 

Fig.  17.  Eye-lash  embedded  in  scar-tissue  within  the  cornea,  and  sur- 
rounded by  epitheloid  cells.     C.  Eye-lash 37 

Fig.  18.  Blood-vessels  of  the  sclerotic  from  a  wounded  eye  in  the  process  of 
phthisis  bulbi.  A.  Proliferation  of  the  endothelial  cells,  i.  Giant- 
cells.     B.  Transformation  into  connective-tissue 46 

Fig.  19.  Corneo-scleral  staphyloma,  i.  New  insertion  of  the  iris  which 
adheres  to  Descemet's  membrane  by  means  of  a  tissue  formed  from  the 
endothelial  cells.  2.  The  ectatic  part ;  the  membrana  Descemetii  has 
disappeared 48 

Fig.  20.  Ciliary  staphyloma.     Ciliary  body  adherent  to  the  sclerotic   and 

atrophic.     Beginning  ectasia 49 


xiv  ^LL  USTRA  TIONS. 


PAGE 


Fig.  21.  Posterior  staphyloma  from  a  myopic  eye.     Choroid  and  sclerotic 

adhere  to  each  oiher  and  are  atrophic 50 

Fig.  22.  Scar  in  the  sclerotic 52 

Fig.  23.  A  small  piece  of  iron  embedded  in  the  sclerotic 53 

Fig.  24.  Trachoma-granule  from  the  bulbar  conjunctiva.  Blood-vessels  in- 
jected with  a  stained  fluid.     L.   Enlarged  lymph-canals 62 

Fig.  25.  Crystalline  lens  dislocated  under  the  conjunctiva  and  there  encap- 

suled 64 

Fig.  26.  Lymphangiectasia  of  the  bulbar  conjunctiva 66 

Fig.  27.  Granuloma  (polypus)  of  the  bulbar  conjunctiva 67 

Fig.  28.  Dermoid  tumor  of  the  bulbar  conjunctiva 6S 

Fig.  29.  Partially  pigmented  epithelial  papillae  from  a  dermoid   tumor  of 

the  bulbar  conjunctiva 71 

Fig.  30.  Meianosarcoma  of  the  bulbar  conjunctiva.  I.  Shows  how  the  pig- 
mented cells  creep  along  the  blood-vessels  of  the  conjunctiva  and  upon 

Bowman's  layer  under  the  epithelium  of  the  cornea 73 

Fig.  31.  Epithelioma  of  the  bulbar  conjunctiva 75 

Fig.  32.  Epithelioma  of  the  bulbar  conjunctiva,     i.  Epithelial  cylinder  filled 

with  round  cells.    2.  Epithelial  cylinders  ending  in  round-cellcylinders. 

Fig.  33.  Epithelioma  of  the  bulbar  conjunctiva.     The  tissue  of  the  cornea 

is  changed  into  one  consisting  of  long  fine  spindle-cells 78 

Fig.  34.  Epithelioma  of  the  bulbar  conjunctiva.  The  tumor  has  perforated 
the  cornea,  and  is  spreading  upon  the  surface  and  into  the  parenchyma 

of  the  iris.     C.  Cornea.     I.  Iris .  .      78 

Fig.  35.  Epithelioma  of  the  bulbar  conjunctiva.  An  anterior  ciliary  artery 
surrounded  by  epithelial  cells.     Nests  of  epithelial  cells  in  the  tissue  of 

the  ciliary  body 79 

Fig.  36.  Serous  iritis.  The  pupillary  edge  of  the  iris  is  adherent  to  the 
anterior  lens-capsule.     The  peripheral  parts  of  the  iris  are  protruding 

into  the  anterior  chamber  (crater-shaped  iris) 85 

Fig.  37.  Hsemorrhagic  iritis  (with  spongy  exudation).  Haemorrhages  in 
the  parenchyma  of  the  iris.     In  the  anterior  chamber  lies  a    fibrinous 

and  a  gelatinous  exudation 87 

Fig.  38.  Plastic  iritis.     Pupillary  membrane 88 

Fig.  39.  Plastic  iritis.  New-formed  connective-tissue  upon  the  anterior 
surface  of  the  iris.     This  tissue  is  lamellar  and  contains  blood-vessels. 

H.  A  large  haemorrhage 89 

Fig.  40.  Purulent  ii  itis 90 

Fig.  41.  New-formed  connective-tissue  uniting  the  posterior  surface  of  the 

iris  with  the  anterior  lens-capsule  after  plastic  iritis 92 

Fig.  42.  Iritis  chronica.     Atrophy  of  the  iris  and  colloid  metamorphosis  of 

its  anterior  endothelial  coat 93 

Fig.  43.  So-called  cyst  of  the  iris,  formed  after  an  injury  to  the  cornea.  The 
walls  of  the  cyst  are  formed  by  Decemet's  membrane,  the  atrophic  iris 
and  some  new-formed  connective-tissue,  and  lined  with  the  endothelium 

of  the  anterior  chamber 95 

Fig.  44.  Incarcerated  iris.     Small  prolapse  of  the  iris  into  a  corneal  wound 

covered  with  new-formed  connective-tissue  and  epithelium gft 


ILLUSTRATIONS.  XV 

PAGE 

Fig.  45.  Traumatic  granuloma  of  the  iris  after  this  membrane  has  prolapsed. 
Gr.  Granuloma.  C.  Cornea.  D.  Descemet's  membrane.  Ir.  Iri^.  Cc. 
Ciliary  body.     LK.  Lens-capsule 98 

Fig.  46.  Ciliary  body  from  a  myopic  eye 100 

Fig.  47.  Ciliary  body  from  an  hypermetropic  eye 100 

Fig.  48.  Sero-fibrinous  cyclilis.     Amorphous  fibrine,  containing  numerous 

round-cells,  lies  upon  the  posterior  lens-capsule 104 

Fig.  49.  Serous  cyclitis.     The  exudation  lies  in  the  tissue  of  the   ciliary 

body  itself,  and  presses  the  muscular  fibres  apart 105 

Fig.  50.  Plastic  cyclitis.     Cyclitic  membrane  upon  the  posterior  lens-capsule. 

Theposterior  chamber  is  obliterated.  Lens  and  iris  are  pressed  forward .    106 

Fig.  51.  Plastic  cyclitis.  Shows  how  the  cells  of  the  retinal  layer  of  the 
ciliary  body  are  changed  into  spindle-cells  and  aid  in  the  formation  of 
a  cycliiic  membrane 107 

Fig.  52.  Plastic  cyclitis.     Tubular  excrescences  of  the   pigmented   (uveal) 

layer  of  the  ciliary  body 107 

Fig.  53.  Plastic   cyclitis.     The   same   tubular   excrescences.     The  younger 

ones  as  yet  unpigmented 108 

Fig.  54.  Plastic  cyclitis.  Cyclitic  membrane.  Detachment  of  the  ciliary  body.   109 

Fig.  55.  Purulent  cyclitis no 

Fig.  56.  Gumma  of  the  ciliary  body.     I.  Iris.     L.  Lens.     G.  Gumma.     Cm. 

Cyclitic  membrane in 

Fig.  57.  Plastic  cyclitis  from  an  eye  with  anterior  phthisis.  The  cyclitic 
membrane  is  very  considerably  shrunken,  and  brings  the  ciliary  bodies 
nearly  in  contact  with  each  other II2 

Fig.  58.  Hypertrophy  of  the  ciliary  muscle  in  a  case  of  cyclitis ...   113 

Fig.  59.  Isolated  rupture  of  the  ciliary  body.  The  eye  was  enucleated  on 
account  of  hsemophthalmus.  The  tissue  of  the  ciliary  body  was  per- 
fectly filled  with  blood.  (The  latter  has  not  been  drawn,  to  show  the 
rupture  better) 1 14 

Fig.  60.  Primary  melanosarcoma  of  the  ciliary  body 115 

Fig.  6r.  Normal  entrance  of  the  optic  nerve  into  the  eye-ball.  i.  A  blood- 
vessel coming  from  the  choroid  and  entering  the  retina iiS 

Fig.  62.  Thickened  and  hardened  intercellular  substance  from  the  pig- 
mented epithelial  layer,  lying  upon  the  lamina  vitrea  of  the  choroid. 
The  pigmented  epithelial  cells  have  been  brushed  off I2i 

Fig.  63.  Vitreous  bodies  upon  the  lamina  vitrea  of  the  choroid  ;  i,  contain- 
ing lime I2i 

Fig.  64.  Formation  of  osseous  tissue  in  the  vitreous  bodies  of  the  lamina 

vitrea  choroidese 122 

Fig.  65.  Tumor-like  new  formation  of  pigmented  and  unpigmented  cell- 
cylinders,  starting  from  the  uveal  layer  of  the  ciliary  body  and  neigh- 
boring choroid   123 

Fig.  66.  Pigmentary  retinitis.  Pigmented  cell-cylinders  going  over  in  such 
cylinders  without  pigment.  Blood-vessel  changed  into  connective- 
tissue 124 

Fig.  67.  Pigmentary  retinitis.     Pigment    in    the   perivascular   sheath  of  a 

retinal  blood-vessel 125 


xvi  ILL  US  TRA  TIONS. 


PAGE 


Fig.  68.  Plastic  choroiditis.     Fibro-cellular  exudation  in  the  tissue  of  the 

choroid 128 

Fig.  69.  Plastic  choroiditis.     Adhesion  between  retina  and  choroid 129 

Fig.  70.  Plastic  choroiditis.     Pigmentation  of  the  retina 129 

Fig.  71.  Purulent  choroiditis 130 

Fig.  72.   Tubercle  of  the  choroid 131 

Fig.  73.  Osseous  tissue,  with  marrow  in  the  choroid 132 

Fig.  74.  Parenchymatous  hsemorrhage  splitting  the  choroid  into  two  layers, 

caused  by  contusion  of  the  eye-ball 136 

Fig.  75.  Granulation-tissue  starting  from  the  wounded  choroid 137 

Fig.  76.  Cystoid  formation  in  the  choroid 138 

Fig.  77.  From  a  chondrosarcoma  of  the  choroid,  i.  Sarcoma-cells.  2. 
Cartilage-tissue  ;  in  its  centre.  3.  Remains  of  the  vitreous  body 
changed  into  delicate,  myxomatous  tissue.  4.  Connective-tissue  sur- 
rounding the  cartilage-tissue  ... 140 

Fig.  78.  Osseous  tissue  formed  in  a  sarcomatous  tumor  of  the  choroid 141 

Fig.  79.  Shows  how  the  double-contoured  nerve-fibres  of  the  optic  nerve 

are  changed  into  non-medullated  ones  in  an  hypermetropic  eye 145 

Fig.  80.  Shows  how  the  double-contoured  nerve-fibres  of  the  opticus  are 

changed  into  non-medullated  ones  in  a  myopic  eye 145 

Fig.  81.  Qidema  of  the  intervaginal  space  and  optic  papilla,     i.  The  en- 
larged intervaginal  space.  2.  Spaces  in  the  optic  papilla  filled  with  serum.   148 
Fig.  82.  Fibrinous   vaginitis    of  the   optic   nerve.      I.  Intervaginal   space 

obliterated  by  new-formed  connective-tissue.     Optic  nerve  atrophic  . . .    149 
Fig.  83.  Interstitial  inflammation  of  the  optic  nerve.     Longitudinal  section.  151 
Fig.  84.  Interstitial  inflammation  of  the  optic  nerve.     Transverse  section  .  .    151 
Fig.  85.  Atrophic  excavation  of  the  optic  papilla  filled  with  a  delicate  con- 
nective-tissue formed  in  the  neighboring  vitreous  body 154 

Fig.  86.  Very  deep  glaucomatous  excavation.     Atrophy  of  the  optic  nerve  .    156 
Fig.  87.  From  an  atrophic  optic  nerve.     Hypertrophy  of  the  connective- 
tissue,  M'hich  contains  some  pigment.     The  nerve- fibres  are  broken  up 

into  a  grumous  substance 157 

Fig.  88.  Granuloma  of  the  optic  papilla 1158 

Fig.  8g.  Cystoid  degeneration  of  the  retina  near  the  ora  serrata 166 

Fig.  90.  Albuminuric  retinitis,    i.  Nerve  fibre  layer,  considerably  thickened 

through  sclerosed  hypertrophic  nerve  fibyes.     2.  Haemorrhage 171 

Fig.  91.  Albuminuric  retinitis.  I.  Outer  granular  layer.  2.  Inner  granular 
layer.  3.  Cavity  filled  with  fil^rine.  4.  Cavity  filled  with  cells  con- 
taining fat-granules.  Both  cavities  containing,  moreover,  peculiar  struc- 
tures of  varying  size,  which  coalesce  and  refract  the  light  very  strongly. 

Some  fat-granule  cells  lie  in  the  outer  granular  layer 172 

Fig.  92.  Detached  and  perfectly  atrophied  retina.     Capillaries  changed  into 

cylinders  of  amorphous  lime 180 

Fig.  93.  Anterior  polar  cataract.  The  apex  of  the  cone  is  formed  by  a 
lamellar,  dim  tissue,  without  any  cellular  elements.     The  basis  consists 

of  lime  and  fat 194 

Fig.  94.  Connective-tissue  within  the  ruptured  lens-capsule 196 

Fig.  95.  Osseous  tissue  formed  within  the  ruptured  lens-capsule 197 


THE    HUMAN    EYE. 


I. 

CORNEA. 

I.  Normal  Conditions. 

The  tissue  of  the  cornea  consists  of  the  following  parts, 
viz.,  the  epithelium,  Reicherfs  or,  as  it  is  commonly  styled, 
Bowman  s  layer,  the  parenchyma,  Descemef  s  membrane  and 
its  endothelium,  blood  and  lymphatic  vessels  and  nerves. 

The  epithelial  layer  of  the  cornea  viewed  from  the  surface 
presents  a  delicate  mosaic,  formed  of  cells  some  of  which 
angular,  and  others  round.  Each  of  these  cells  possesses  a 
large,  round  or  oval  nucleus,  in  which  usually  several  nucleoli 
may  be  seen.  A  small  amount  of  cementing  substance 
unites  the  cells  with  each  other,  and  can  be  easily  demon- 
strated by  staining  the  cornea  with  nitrate  of  silver  or  chloride 
of  gold. 

In  teased  specimens  of  this  superficial  part  of  the  corneal 
epithelium  we  frequently  find  such  cells  lying  on  their  edge. 
They  then  appear  considerably  broader  around  the  nucleus, 
not  unlike  the  blood-corpuscles  of  the  amphibia  {Waldeyer). 

These  flattened  cells  form  several  layers. 

Beneath  them  follow  several  layers  of  cells,  characterized 
by  being  less  flattened  and  bearing  offsets.  Of  these  we 
have  again  two  distinct  kinds.  The  one  bear  small  offsets  all 
over  their  surface — serrated  cells — and  the  other  have  only 
one,  two  or  three  broader  offsets  on  their  inner  surface.  The 
small  offsets  of  the  former,  which  lie  more  superficially,  in- 
terlace with  each  other.  The  large  offsets  of  the  latter,  which 
lie  nearer  to  Bowman  s  layer,  dip  into  the  interstitia  between 
the  cells  of  the  underlying  layer.     Each  of  these  cells  again 


2  THE  HUMAN'  E  YE. 

has  a  large  round  or  oval  nucleus  with  several  nucleoli. 
I  often  also  found  in  this  layer  cells  with  two  nuclei  and 
smaller  ones  of  apparently  recent  date.  The  same  cementing 
substance  which  unites  the  cells  of  the  superficial  layer,  is 
also  found  between  these. 

The  innermost  part  of  the  epithelium  is  formed  of  one 
single  layer,  called  the  basal  layer.  Its  cells  are  long  and 
cylindric  or  club-shaped.  Their  form,  however,  varies  greatly. 
Sometimes  they  are  broader  in  their  outer  and  sometimes  in 
their  inner  part ;  some  are  cone-shaped,  while  others  have  one 
or  two  notches,  in  which  the  neighboring  cells  fit.  They 
all  have  a  round  or  oval  nucleus  with  nucleoli ;  some  of  them 
also  have  two  nuclei  {Waldeyer).  These  cells,  too,  are  united 
by  the  same  cementing  substance,  and  thus  all  the  different 
layers  of  the  epithelium  are  united  into  one. 

Waldeyer  is  of  the  opinion,  that  the  new  formation  of 
epithelial  cells  takes  place  in  the  basal  and  middle  layers. 
The  corneal  epithelium,  however,  consists  altogether  of  living 
cells,  as  even  the  most  superficial  ones  have  a  nucleus,  and  I 
therefore  see  no  sufficient  reason  for  denying  to  one  of  these 
layers  the  ability  of  producing  new  cells,  y.  Arnold's  experi- 
ments on  the  regeneration  of  epithelial  defects  of  the  cornea, 
moreover,  decidedly  prove  that  the  new  formation  takes 
place  in  all  the  layers. 

Under  the  epilhelium  of  the  cornea  lies  Reicherfs  or 
Bowman  s  layer.  This  appears  as  a  vitreous  layer,  which  is, 
however,  not  distinctly  separated  from  the  underlying  paren- 
chyma. A  high  magnifying  power  shows  it  to  be  somewhat 
striated,  and  we  may  split  it  into  fibrillae  by  a  number  of 
chemical  agents  {Waldeyer^.  I  never  found  cells  in  this 
layer  in  its  normal  condition.  Boivmans  layer  cannot  be 
readily  and  evenly  separated  from  the  underlying  paren- 
chyma, as  fibres  springing  from  it  pass  into  the  latter,  and 
vice  versa.  They  can  be  readily  traced  between  the  lam- 
ellae of  the  parenchyma.  They  also  were  first  described 
by  Bowman. 

At  the  periphery  of  the  cornea  Bozvmatis  layer  is  split 
up  into  its  fibrillar,  and  these  pass  over  into  the  conjunc- 
tival tissue. 


CORNEA.  2 

Waldeyers  opinion  that  Bowman  s  layer  is  condensed 
parenchyma  of  the  cornea,  and  not  a  separate  membrane,  is 
certainly  correct.  In  the  following  we  shall  have  to  state 
additional  reasons  for  this  assertion. 

Some  few  authors  maintain  that  the  outer  surface  of 
Bowman  s  layer  bears  small  elevations  in  which  the  cells  of 
the  basal  layer  of  the  epithelium  are  said  to  fit. 

The  parenchyma  proper  of  the  cornea  consists  of  the 
stroma,  embedded  in  which  lies  a  system  of  lymphatic  canals, 
the  cellular  elements,  blood  vessels  and  nerves  of  the  cornea. 

The  stroma  of  the  corneal  parenchyma  is  transparent  and 
formed  of  exceedingly  fine  fibrillae,  which  are  united  by  a 
cementing  substance.  When  isolated  the  fibrillae  appear 
wavy,  but  otherwise  in  no  way  different  from  connective  tissue 
fibrillae.  I  have  never  found  elastic  fibrillae  among  them 
{Henle).  The  best  agent  to  split  the  cornea  into  these  fibrillae, 
is  a  ten  per  cent,  solution  of  common  salt  {Schweigger-Seidel). 
Sometimes  I  obtained  a  good  view  of  them  in  situ  by  stain- 
ing the  cornea  with  logwood.  It  then  became  evident  that 
the  fibrillae  intersect  each  other  at  all  possible  angles,  and 
not  at  right  angles  only,  as  Waldeyer  and  others  maintain. 

These  finest  fibrillae  of  the  corneal  stroma  are  united  into 
fascicles,  and  several  of  these  fascicles  together  form  a  lamella. 
The  lamellae  lie  mostly  parallel  to  the  surface  of  the  cornea, 
from  which  rule  exceptions  are  rare. 

Fibrills,  fascicles  and  lamellae  are  united  with  each  other 
by  a  protaplasmatic  cementing  substance,  which  is  seen  as  a 
fine  homogeneous  light  streak  between  them,  and  has  some- 
times a  granular  appearance.  We  have  thus  an  interfibrillar, 
an  interfascicular  and  an  interlamellar  but  always  the  same 
cementing  substance. 

Embedded  in  this  substance,  furthermore,  are  von  Reck- 
lingJiausen  s  corneal  canals.  It  is  well  known  that,  by  stain- 
ing the  living  cornea  with  nitrate  of  silver  or  chloride  of  gold, 
these  canals  are  easily  demonstrated.  Logwood  and  carmine 
do  not  answer  this  purpose  very  well.  Berlin  blue  some- 
times, but  not  constantly,  yielded  me  as  good  pictures  as 
gold  or  silver.  In  a  plain  view  of  the  cornea  thus  stained, 
we  see  a  system  of  fine  canals  which  intersect  each  other  at 


4  THE  HUMAN  E  YE. 

very  varying  angles,  and  which  form  here  and  there  a  larger 
cavity,  which  is  called  a  lacuna.  In  transverse  sections  of 
the  cornea  we  see  that  this  system  of  canals  (like  the  lamellae) 
runs  mostly  in  a  direction  parallel  to  the  outer  surface  of  the 
cornea,  and  that  the  lacunae  are  arranged  in  rows  lying,  of 
course,  in  the  same  direction.  The  small  canals,  however, 
which  unite  the  lacunae  of  the  larger  canals  with  each  other, 
pass  through  the  corneal  parenchyma  at  very  different  angles. 
In  transverse  sections  taken  from  hardened  specimens  the 
lacunae  appear  lens-shaped.  From  the  plain  views  of  a 
stained  living  cornea  we  know,  however,  that  their  shape 
varies  considerably,  according  to  the  number  of  canals  which 
are  in  connection  with  them. 

The  caliber  of  the  canals  and  lacunae  is  by  no  means  uni- 
form. As  a  rule,  however,  as  pointed  out  by  von  Reckling- 
hausen and  confirmed  by  Waldeyer,  the  canals  and  lacunae 
which  lie  nearest  to  Bowman's  layer  are  the  narrowest, 
while  those  lying  nearest  to  Descemefs  membrane  are  the 
widest.  The  same  rule  holds  good  with  regard  to  the  thick- 
ness of  the  lamellae  in  these  parts  of  the  cornea.  Waldeyer 
and  other  authors  before  and  with  him  have  drawn  the  at- 
tention to  these  facts,  and  to  the  probability  that  the  cornea 
consists  of  a  conjunctival,  a  sclerotical  and  a  choroideal 
part.  We  would  thus  find  the  widest  canals  and  lacunae  in 
the  choroideal  and  the  smallest  in  the  conjunctival  part  of 
the  cornea. 

Another  means  of  demonstrating  this  system  of  canals 
and  lacunae,  is  to  inject  into  them  a  colored  fluid.  Bowman 
while  experimenting  on  the  cornea  of  animals  obtained  by 
such  injection  a  system  of  straight  canals,  which  he  called 
corneal  tubes.  As  far  as  my  experiments  show,  these  corneal 
tubes  do  not  belong  to  the  human  cornea.  Waldeyer  suc- 
ceeded in  injecting  a  colored  fluid  into  the  interlamellar  and 
interfascicular  canals.  Since  I  could  not  procure  Waldeyer  s 
fluids  in  the  proper  condition,  I  made  my  injections  with  a 
saturated  solution  of  Berlin  blue.  I  thus  not  only  obtained 
injections  of  the  canals  lying  in  the  interlamellar  and  inter- 
fascicular cementing  substance  (as  Waldeyer)^  but,  moreover, 
a  system  of  blue  lines  corresponding  exactly  with  the  ar- 


CORNEA.  5 

rangement  of  the  fibrillae,  as  I  had  sometimes  occasion  to 
see  it  after  staining  the  cornea  with  logwood.  These  lines 
(See  Fig.  i)  were  arranged  in 
fascicles  intersecting  each  other 
at  various  angles.  I  think,  if  I 
am  not  mistaken,  that  I  have 
thus  injected  also  the  interfibril- 
lae  canals,  which,  of  course,  were 
somewhat  enlarged  by  the  pres- 
sure exerted  upon  them  during 
the  injection.  This  system  of  in- 
terfibrillar  canals  is  in  direct  con-  ^  ^igr- 1.  d)  The  interfibniiar  canals.  (2, 

Interlamellar  and    lacunre.    N.    Nerve- 
nection    with     the    interfascicular    sheath  filled  with  the  injection-fluid. 

and  interlamellar  canals,  and  all  of  them,  as  we  shall  see 
later  on,  are  in  direct  communication  with  the  canals  en- 
closing the  corneal  nerves.     (See  Fig  i.) 

Kuehne  and  others  describe  this  system  of  canals  as  being 
filled  with  a  continuous  protoplasmatic  substance.  Most  au- 
thors, however,  resent  this  opinion.  Von  Recklinghausen  and 
others  after  him,  whose  opinion  I,  too,  share,  maintain  that 
these  canals  contain  the  nutritive  (lympathic)  fluid. 

The  canals  have  no  walls  of  their  own  (  Waldeyer).  Con- 
trary statements  seem  to  be  erroneous. 

Besides  the  nutritive  fluid,  which  fills  the  canals  through- 
out, they  contain  three  different  kinds  of  cells,  viz  :  fixed  cor- 
neal cells,  wandering  (lymphatic)  cells,  and  pigmented  cells. 

The. fixed  cells  of  the  cornea,  as  they  have  been  called  by 
Co/mheim,  lie  in  the  lacunae.  Such  a  cell,  however,  never 
altogether  fills  the  lacuna,  in  which  it  lies.  They  mostly 
adhere  to  one  wall  of  the  lacuna,  and  fill  only  about  two- 
thirds  of  it.  The  cells  appear  as  protoplasmatic  bodies  with 
an  oval  or  round  nucleus,  usually  containing  several  nucleoli. 
The  protoplasma  is  very  granular  around  the  nucleus.  Wal- 
deyer succeeded  in  isolating  these  cells,  and  described  them  as 
very  thin,  completely  flattened  bodies,  having  a  few  short 
offsets.  I  have  never  been  able  to  isolate  them.  I,  how- 
ever, frequently  found  their  nucleus  perfectly  hidden  by  the 
granular  protoplasma,  which  fact  would  prove  that  these  cells 
are  not  always  flat,  but  sometimes  thicker  around  their  nucleus. 


6  THE  HUMAN  EYE. 

Besides  the  agents  recommended  by  Waldeyer  and  com- 
monly used  in  studying  these  parts,  I  can  recommend  the 
staining  of  the  cornea  with  eosine  {Dreschfeld),  an  aniline 
color  which  is  highly  fluorescent.  This  fluorescence  causes 
the  outlines  of  the  cells,  etc.,  to  be  exceedingly  well  defined. 

The  offsets  of  a  fixed  corneal  cell  reach  only  a  very  small 
distance  into  the  canals  which  communicate  with  the  lacuna 
in  which  it  lies. 

A  number  of  undoubted  observations  are  on  record  which 
prove  the  contractility  of  the  fixed  corneal  cells,  and  Waldeyer 
lately  has  seen  them  move  about  along  the  walls  of  the  lacuna. 

The  pigmented  cells  which  we  sometimes  find  in  the  per- 
iphery of  the  cornea  (especially  in  the  eyes  of  negroes)  are 
perfectly  identical  with  these  unpigmented  fixed  corneal  cells. 
Their  granular  pigment  is  enclosed  in  the  protoplasma,  leav- 
ing the  nucleus  free. 

Besides  the  fixed  cells  we  always  find  in  the  cornea  a 
number  of  wandering  (lymphatic)  cells.  They  differ  in  no 
way  from  those  found  in  other  organs,  and  they  wander 
along  the  preformed  corneal  canals,  and  not  promiscuously 
through  the  tissue.  This  is  proven  beyond  doubt  by  Gener- 
sicJts  experiments,  who  brought  living  cornese  into  the  lymph- 
sacs  of  frogs.  1  have  often  repeated  this  experiment,  and 
.  always  with  the  same  result,  that  is  of  finding  the  immigrated 
lymph-cells  filHng  only  the  corneal  canals.  The  same  is  seen 
in  the  earlier  stages  of  inflammation  of  the  cornea,  when  the 
structure  of  its  parenchyma  has  not  yet  been  destroyed. 

The  connection  between  fixed  and  wandering  cells  in  the 
corneal  parenchyma  is  not  yet  clearly  defined.  I  can  fully 
confirm  the  opinions  of  earlier  authors,  that  fixed  cells  can 
become  wandering  ones.  Whether,  however,  wandering  cells 
can  become  fixed  ones,  is  as  yet  an  open  question. 

The  parenchyma  of  the  cornea  is  covered  on  its  inner 
surface  by  Desccmcfs  membrane.  This  membrane  is  a  per- 
fectly homogeneous,  vitreous  membrane,  and  is  about  two- 
thirds  the  thickness  of  Bozvnians  layer.  I  cannot  agree  with 
those  authors  who  state  it  to  have  in  transverse  sections 
a  striated  appearance.  No  more  can  I  concur  in  Waldeyer  s 
opinion,  who  says  that  Descemefs  membrane  cannot  readily 


CORNEA.  7 

be  separated  from  the  corneal  parenchyma.  Pathological 
specimens  have  taught  me  that  a  perfect  detachment  of  this 
membrane  is  possible.  Walb  had  also  occasion  to  describe 
such  a  case. 

Descemef s  membrane  is  moreover  an  elastic  membrane. 
In  a  previous  paper  I  have  stated  its  tendency  to  wind  itself 
up  in  a  spiral  way  from  specimens  of  the  animal  eye.  I  can 
add  now  that  I  am  in  possession  of  specimens  from  the 
human  eye  in  which  Descemef s  membrane  is  detached  and 
shows  three  and  four  spiral  windings.  This  detachment  and 
the  tendency  to  wind  itself  up  spirally  seem  to  me  to  prove 
that,  unlike  Bowman  s  layer,  this  membrane  is  really  a  sep- 
arate structure,  and  not  condensed  corneal  parenchyma, 
as  Waldeyer  seems  to  think.  This  similarity  between  Des~ 
cemet" s  membrane  and  the  vitreous  membrane  of  the  choroid, 
besides  other  similarities  mentioned  later,  seems  to  confirm 
the  opinion  that  the  inner  portion  of  the  cornea  is  really  its 
choroideal  part. 

The  inner  surface  of  Descemef  s  membrane  is  covered 
by  a  single  layer  of  endothelial  cells.  These  cells  are  not  as 
regular  and  uniform  in  shape  and  size  in  the  human  eye  as  they 
usually  are  in  the  eyes  of  animals.  They  are  five  or  six  in  num- 
ber, angular,  or  round,  and  have  a  round  or  eliptical,  sometimes 
bean-shaped  nucleus,  with  one  or  more  nucleoli.  In  trans- 
verse sections  they  often  appear  so  flat  that  the  thin  layer  is 
only  recognized  with  difficulty,  in  other  eyes  they  appear  as 
large  cuboid  cells  with  a  round  nucleus.  They  are  united 
by  a  cementing  substance,  not  different  from  the  one  de- 
scribed in  other  parts  of  the  cornea.  In  the  angles  between 
two  or  three  neighboring  cells,  we  frequently  find  stomata. 
Near  the  periphery  of  Descemef s  membrane  I  nearly  always 
find,  like  Henle,  the  "  vitreous  warts,"  which  were  first  describ- 
ed by  Hassal.  I  found  them  several  times  even  in  children's 
eyes,  which  proves  that  the  opinion  of  Waldeyer  and  others 
who  consider  these  "  warts,"  to  be  a  change  caused  by  old 
age  only  is  erroneous.  They  are  round,  vitreous  bodies, 
sometimes  granular,  mostly  perfectly  homogeneous.  Some- 
times two  or  more  of  them  coalesce,  just  as  we  shall  describe 
later  on  of  the  vitreous  (colloid)  bodies  of  the  lamina  vitrea 


8 


THE  HUMAN  E  YE. 


of  the  choroid.  They  generally  push  the  adjacent  endothel- 
ial cells  aside,  and  alter  their  shape  accordingly.  They  are 
seldom  as  large  as  the  endothelial  cells,  are  very  hard,  and 
resist  all  chemical  agents. 

At  the  corneo  scleral-margin,  the  region  where  cornea 
and  sclerotic  pass  over  into  each  other,  the  tissues  show  cer- 
tain characteristic  alterations. 


Fig.  2.  Corneo-scleral  margin.  C.  Cornea.  S.  Sclerotic.  OS.  Schlemm's  canal.  D.  Des- 
cemet's  membrane.  I.  Iris.  Lp.  The  fibres  of  the  ligamentum  pectinatum  with  endo- 
thelial cells  adhering  to  them. 

The  corneal  epithelium  passes  directly  over  into  the  con- 
junctival epithelium.  The  fibres  into  \\\{\c\i  Bowman  s  layer, 
is,  split  up  and  the  anterior  lamellae  of  the  corneal  paren- 
chyma together  enter  the  subconjunctival  (episcleral)  tissue 
in  such  a  way  that  these  two  parts  cannot  be  separated  with- 
out tearing  the  fibres.  (This  is  the  so-called  conjunctival 
part  of  the  cornea.) 


CORNEA.  g 

The  bulk  of  the  corneal  lamellae  terminate  in  the  lam- 
ellae and  fibres  of  the  sclerotic,  from  which  they  are  not  his- 
tologically, but  chemically,  different.  The  corneal  canals  also 
are  continuous  with  those  of  the  sclerotic  {Waldeyer).  (This 
is  the  scleral  part  of  the  cornea). 

Descemefs  membrane  and  the  adjacent  lamellae  undergo 
very  important  changes  in  this  region.  Waldeyer,  when  de- 
scribing these  parts,  states  that  none  of  the  previous  illus- 
trations gave  an  exact  picture  of  these  conditions,  and  I 
must  add  that  his  own  does  not  do  so  either.  The  illustra- 
tion herewith  given  (See  Fig.  2)  shows  these  conditions  still 
better.  It  is  drawn  from  a  specimen  taken  from  the  myopic 
eye  of  an  adult.  We  here  plainly  see  that  Descemefs  mem- 
brane and  the  adjacent  lamellae  are  split  up  into  fibres,  which 
are  partially  lost  in  the  tendon  and  connective  tissue  of  the 
ciliary  muscles  and  partially  in  the  tissue  of  the  iris.  Ad- 
herent to  these  fibres  are  a  number  of  endothelial  cells  which 
appear  very  similar  to  those  covering  the  posterior  surface 
of  Descemefs  membrane.  Between  the  fibres  are  open  cavi- 
ties and  canals  which  com- 
municate on  one  side  with 
the  anterior  chamber,  on  the 
other  with  Schlemtns  canal. 
This  system  of  cavities  and 
canals  is  called  Font  ana  s 
spaces.  While  in  the  ani- 
mal eye  these  spaces  are 
covered   by  what  has  been 

styled    the    "  iris-trabeculae  "     '''^•S-  isolated  fibres  of  the  ligamentum  pec- 
-'  tinatum.    The  endothelial  cells  are  shrunken 

(Irisbalken),  such    trabeculae       and  appear  as  darker  swellings. 

springing  from  the  iris  are  not  found  in  the  human  eye. 
The  network  of  fibres  formed  in  this  region  through  the 
splitting  up  of  Descemefs  membrane,  has  been  called  the 
ligamentum  pectinatum.  In  hardened  specimens  it  can  be 
detached  with  the  periphery  of  Descemefs  membrane,  and  we 
then  find  what  Fig.  3  illustrates ;  a  network  of  coarse  con- 
nective-tissue fibres,  which  refract  the  light  strongly,  and 
have  therefore  a  peculiar  sclerotic  appearance,  to  which 
a  number  of  endothelial  cells  are  adherent.     This   network 


lO  THE  HUMAN  EYE. 

passes  over  into  Desceniefs  membrane  on  one  side,  on  the 
other,  as  stated  above,  in  the  iris  and  ciliary  body.  Its 
outer  part  terminates  in  a  fascicle  of  circular  equatorial 
fibres,  forming  a  ring  which  has  received  the  name  of  the 
posterior  terminal  ring  {Gre^izring).  Besides  this  there  ex- 
ists, but  less  constantly,  an  anterior  terminal  ring  nearer  the 
place  where  Descemef  s  membrane  begins  to  be  split  up  into 
fibres. 

The  blood-vessels  of  the  cornea  He  only  in  its  most  periph- 
eral parts,  and  form  a  small  border  at  the  corneo-scleral 
margin  which  varies  in  breadth  from  one  to  two  and  a  half 
mm.  This  difference  in  breadth  is  found  in  nearly  every 
individual  cornea. 

These  corneal  blood-vessels  come  from  the  anterior  ciliary 
arteries,  and  anastomose  with  the  marginal  blood-vessels  of 
the  conjunctiva,  which  have  the  same  origin.  The  superficial 
arterial  branches  of  the  marginal  blood-vessels  very  soon, 
after  having  entered  the  cornea,  end  in  a  capillary  network 
which  forms  the  so-called  marginal  loops  of  the  cornea.  Leber, 
in  Graefe  and  SaemiscJis  cyclopedia,  gives  an  excellent  illus- 
tration of  these  blood-vessels.  I  frequently  found,  however, 
that  these  terminal  loops  when  injected  with  a  colored  fluid 
have  little  cone  or  diverticle-like  offsets,  in  the  direction 
towards  the  centre  of  the  cornea,  which  are,  perhaps,  remains 
of  the  foetal  praecorneal  blood-vessels,  and  certainly  must  be 
of  great  importance  for  the  pathological  new-formation  of 
blood-vessels  in  this  membrane.  In  the  inner  layers  of  the 
cornea  the  capillary  network  passes  over  into  comparatively 
broad  veinous  branches.  The  blood  is  carried  by  them  to 
the  episcleral  and  then  into  the  anterior  ciliary  veins. 

The  blood-vessels  of  the  cornea  are  histologically  in  no 
way  different  from  others. 

At  the  corneo-scleral  margin  from  forty  to  forty-eight 
larger  nerve-branches  enter  the  posterior  layers  of  the  corneal 
tissue.  They  come  partially  from  the  anterior  ciliary,  and 
partially  from  the  conjunctival  nerves.  Very  soon  after 
their  entrance  into  the  cornea  they  lose  their  double  contour. 
They  then  branch  off  and  form  what  is  called  the  "  narrow 
stroma-plexus."     From  this  plexus  smaller  branches  run  for- 


CORNEA.  1 1 

ward,  and  just. behind  Bowman  s  layer  split  again  into  axis- 
cylinders  and  axis-fibrillae,  which  pierce  Bowman's  layer  and 
form  the  "  sub-epithelial  plexus  "  around  the  basis  of  the  basal 
layer  of  the  corneal  epithelium.  From  this  plexus  again 
fibrillae  spring  forward  into  the  anterior  parts  of  the  epithe- 
lium and  there  form  between  the  flattened  cells  the  terminal, 
"  intra-pithelial  "  plexus.  Whether  this  is  really  the  terminal 
plexus,  and  in  what  way  the  fibrillae  end,  is  as  yet  an  open 
question.  Kuehne  and  others  say  that  they  end  in  the  cells. 
Coh7iheim  states  that  they  have  a  special  terminal  nodule 
lying  upon  the  external  surface  of  the  epithelium.  Other 
authors  maintain  a  free  ending  between  the  cells.  My  own 
specimens  did  not  allow  me  a  deciding  opinion  with  regard 
to  this  point. 

I  can,  however,  confirm  the  statement  of  others  that  the 
larger  nerve-branches  lie  in  a  system  of  canals  which  are 
sometimes  lined  with  flat  endothelial  cells.  Where  the 
larger  nerves  are  split  up  into  their  branches,  an  endothelial 
cell  is  often  found  lying  on  the  nerve  itself,  these  have 
been  mistaken  for  ganglionic  cells.  There  are,  however, 
no  ganglionic  cells  to  be  found  in  the  cornea,  in  which  opin- 
ion I  agree  with  Waldeyer.  In  specimens  which  have  been 
stained  with  chloride  of  gold,  the  axis-fibrillae  always  appear 
varicose.  Waldeyer  is  of  the  opinion  that  this  varicosity  is 
artificially  produced,  and  does  not  exist  during  life,  an 
opinion  put  forth  before  him  by  Engelmann. 

It  has  been  stated  before  that  the  system  of  canals  in 
which  the  nervous  fibres  are  embedded  is  in  direct  communi- 
cation with  the  lympathic  canals  of  the  cornea,  which  is 
proven  by  injecting  the  latter  with  a  colored  fluid.  (See 
Fig.  I.) 


2.  Pathological  Conditions. 
A .  Keratitis  and  its  Results. 

The  large  majority  of  the  facts  collected  in  the  following 
pages  is  derived  from  examinations  of  human  eyes. 


12  THE  HUMAN  EYE. 

To  whatever  degree  a  cornea  is  inflamed,  we  find  it 
to  contain  more  cells  than  in  the  normal  condition.  These 
additional  cells  are  chiefly  round-cells  and  partially  small 
spindle-shaped  ones.  They  are  the  same  formative  cells 
which  are  called  either  wandering  or  lymphatic,  and  are 
identical  with  the  emigrated  white  blood-corpuscles  as  we 
find  them  in  the  beginning  in  every  inflamed  tissue. 

CoJinhcim  and  his  pupils  maintain  that  these  cells  are 
all  emigrated  ones  from  the  marginal  blood-vessels  of  the 
cornea.  According  to  Boettcher  and  others  they  are  simply 
the  products  of  the  proliferating  cells  of  the  corneal  paren- 
chyma. My  own  examinations  of  the  inflamed  human  cornea 
and  experiments  on  the  cornea  of  animals,  force  me  to  agree 
with  those  authors  who  believe  that  the  additional  cells,  in  such 
an  inflamed  cornea  take  their  origin  from  both  these  points, 
viz.,  from  the  blood-vessels  and  the  fixed  (and  wandering) 
cells.     {Strieker,  Norris,  Fuchs,  etc.) 

I  am,  furthermore,  convinced  by  my  own  experimental 
researches  that  the  process  of  emigration  of  cells  from  the 
marginal  blood-vessels  precedes  the  process  of  proliferation 
of  the  cells  of  the  corneal  parenchyma.  I  once  saw,  for 
instance,  a  cornea  perfectly  filled  with  round-cells  only  three 
hours  after  a  superficial  injury.  These  cells  could  not  possi- 
bly have  been  the  result  of  proliferation  of  the  corneal  cells, 
and  therefore  could  only  be  immigrated  ones  from  the  blood- 
vessels. These  immigrated  cells  lie,  as  a  rule,  at  first  in  the 
corneal  canals,  not  in  the  lacunae.  Only  when  the  process  of 
proliferation  begins  in  the  fixed  corneal  cells,  we  find  more 
than  one  cell  in  the  lacunae. 

I  have  seen  fixed  corneal  cells,  which  in  this  second  stage 
contained  three  and  four  nuclei.  If  the  process  of  inflamma- 
tion does  not  stop  here,  the  cells  soon  become  so  numerous 
that  the  tissue  of  the  cornea  suffers  under  the  pressure  and 
becomes  gradually  mortified.  This  necrosis  of  the  corneal 
tissue  may  be  confined  to  a  small  intraparenchymatous  space 
(abscess)  or  may  reach  the  surface  (ulcer). 

Whilst  in  the  normal  cornea,  as  we  stated  above,  the 
wandering  cells  lie  in  the  corneal  canals  only  and  not  in  the 
stroma,  the  latter  cannot  resist  their  vital  power  any  longer 


CORNEA. 


13 


in  the  later  periods  of  inflammation,  and  we  then  see  that  the 
new-formed  cells  traverse  the  stroma  of  the  cornea  in  all 
directions,  totally  disregarding  the  corneal  canals. 

We  have  in  the  following  pages  to  speak  of  two  different 
degrees  of  inflammation  of  the  cornea,  viz.,  infiltration-kera- 
titis  and  purulent  keratitis.  These  two  kinds  are,  however, 
different  only  in  degree;  but  they  are  histologically  distinct 
enough  from  each  other.  Under  these  two  heads  we  can, 
furthermore,  place  all  the  manifold  kinds  of  keratitis  which 
the  clinicists  can  and  must  consider  separately,  and  the 
histological  conditions  do  not  allow  us  to  speak  of  more 
than  these  two  kinds  of  inflammation  of  the  cornea. 

a.  Infiltratio7i  of  the  Cornea. 

The  characteristic  feature  of  infiltration  of  the  cornea 
is  the  immigration  (very  rarely  also  the  new  formation)  of 
round-cells  into  the  parenchyma  of  the  cornea.  This  immi- 
gration never  leads  to  a  perfect  destruction  of  the  latter,  and 
only  very  rarely  alters  it  at  all. 

The  infiltration  is  usually  confined  to  only  a  circumscribed 
part  of  the  cornea,  and  never  involves  its  entire  thickness. 

We  find  histologically,  at  first,  only  a  number  of  round- 
cells  filling  the  canals  of  the  diseased  part  of  the  cornea. 
Later  on  we  sometimes  also  see  signs  of  proliferation  in  the 
fixed  corneal  cells.  The  round-cells  lie  chiefly  in  the  inner 
layers  of  the  cornea,  and  infiltration-keratitis  but  seldom 
affects  the  lamellae  which  lie  next  to  Bowmart  s  layer. 
When  the  infiltration  is  confined,  as  is  the  rule,  to  the  inner 
parts  of  the  cornea,  the  epithelium  remains  unaltered ;  if  it 
affects  the  lamellae  nearer  the  surface,  the  epithelium  is 
always  found  in  a  pathological  condition.  It  appears  micros- 
copically in  toto  irregular  and  lacks  its  normal  lustre  and 
smoothness  ;  microscopically  we  find  its  cells  very  irregular  in 
shape,  granular  and  much  enlarged,  so  that  the  whole  of  the 
epithelial  layer  covering  the  infiltrated  portion  of  the  par- 
enchyma is  somewhat  thickened.  This  thickening  may 
furthermore  be  due  to  serous  imbibition  or  to  proliferation 
and  new  formation  of  these  cells.  The  corneal  lamellae  sur- 
rounding the  infiltrated  part  appear  in  no  way  altered. 


14 


THE  HUMAN  E  YE. 


Infiltration  may  heal  by  absorption  of  the  immigrated 
cells  which  may  or  may  not  be  preceded  by  the  formation 
of  new  blood-vessels.  These  blood-vessels  spring  from  the 
marginal  vessels  nearest  the  infiltrated  part.  J.  Arnold  has 
described  the  way  in  which  this  new-formation  takes  place, 
and  I  can  fully  endorse  his  views.  At  first  we  find  small 
protoplasmatic  offsets  growing  from  the  marginal  blood- 
vessels, nearest  the  diseased  part,  which  grow  thicker  as  they 
grow  farther  into  the  corneal  tissue.  Gradually  the  central 
part  of  these  solid  offsets  becomes  hollow,  and  we  find  later 
on  a  protoplasmatic  tube,  with  endothelium  filled  with  a  few 
blood-corpuscles.  Carmalt  and  Strieker  saw  new  blood-ves- 
sels being  formed  out  of  fixed  corneal  cells.  They,  however, 
stand  alone  in  this  experience. 

This  new  formation  of  blood-vessels  generally  begins  in 
the  innermost  layers  of  the  cornea.  Later  on  we  sometimes 
find  blood-vessels  in  the  superficial  layers  too.  The  latter 
is  the  rule  in  cases  of  superficial  infiltration.  The  new- 
formation  of  blood-vessels  is  sometimes  accompanied  by 
hypertrophy  of  the  conjunctival  tissue  at  the  corneal  mar- 
gin, and  the  latter  is  then  found  to  grow  in  between  the 
epithelium  and  Bowman  s  layer,  and  to  be  filled  with  round- 
cells  and  new-formed  blood-vessels.  This  interposed  tissue 
has  lately  been  styled  pannous. 

During  the  process  of  recovery,  the  new-formed  blood- 
vessels either  disappear  or  in  rare  cases,  remain  persistent. 
If  the  latter  is  the  case,  the  larger  ones  generally  have  a  well- 
defined  adventitia. 

Infiltration,  as  stated  above,  but  very  rarely  alters  the 
corneal  parenchyma,  and,  as  a  rule,  leaves  no  trace  behind. 
In  rare  cases  it  leaves  a  scar.  This  is,  however,  always  the 
case  when  infiltration  results,  goes  in  the  purulent  form 
of  keratitis  with  partial  destruction  of  the  corneal  tissue.  If 
the  infiltration  concerns  the  corneo-scleral  tissue,  it  some- 
times produces  sclerosis  of  the  involved  parts,  which  is  then 
the  result  of  the  new-formation  of  translucent  connective 
tissue  between  the  normal,  transparent  lamellae  and  subse 
quent  obliteration  of  the  involved  corneal  canals.  This  pro- 
cess is  not  to  be  confounded  with  that  of  the  formation  of  a 


CORNEA. 


15 


scar,  since  the  new  formation  here  does  not  replace  destroyed 
tissue.  Such  a  new  formation  of  only  translucent  tissue 
takes  place  also  around  those  blood-vessels  which  remain 
persistent,  and  is  the  cause  of  the  grayish  color  of  these  parts. 

We  must  enumerate  under  the  type  of  infiltration-kera- 
titis  the  following  forms  which  clinicists  consider  as  sep- 
arate diseases,  viz.,  corneal  infiltration,  parenchymatous 
keratitis  (which  does  not,  as  a  rule,  show  any  alteration  of 
the  corneal  parenchyma),  pannous  or  vascular  keratitis, 
phyctaenular  keratitis  and  some  forms  of  traumatic  kera- 
.  titis  (results  of  cuts  inflicted  by  sharp  or  ragged-edged 
instruments.) 

Among  the  forms  of  the  clinically  so-called  parenchyma- 
tous keratitis  there  is  one  characterized  by  a  network  of 
systems  of  lines  which  are  distinct  from  the  grayish,  infiltrated 
surrounding  parts  of  the  cornea,  and  cross  each  other  at 
different  angles.  This  network  always  lies  in  the  superficial 
layers,  and  is  seen  when  the  narrow  canals  in  the  superficial 
layers  are  especially  filled  with  round  cells. 

Phyctaenula,  according  to  Iwanoff,  is  a  circumscribed 
infiltration  of  Bowman  s  layer,  and  always  confined  to  the 
parts  surrounding  a  nerve-branch,  piercing  into  the  epithelial 
layer.  This  simple  local  infiltration  generally  results  in 
local  purulent  keratitis,  with  loss  of  substance  and  the  forma- 
tion of  a  scar. 

Among  the  forms  of  traumatic  keratitis  one  has  always 
been  of  special  interest  to  ophthalmologists.  It  has  been 
called  striped  keratitis  (Streifige  keratitis).  This  form  of 
infiltration-keratitis  is  found  after  injuries  (mostly  opera- 
tive) on  the  corneo-scleral  tissue.  We  find  in  such  cases, 
besides  the  general  dimness  of  the  parts  surrounding  the 
wound,  a  number  (generally  from  10  to  12)  grayish  stripes, 
which  start  from  the  wound  in  a  radiating  direction  towards 
the  centre  of  the  cornea,  and  after  nearly  reaching  it  are 
bent  in  the  form  of  arches  and  disappear  in  the  normal 
tissue.  In  order  to  find  the  real  cause  of  this  strange  pic- 
ture, I  made  a  large  number  of  parenchymatous  injections  at 
the  corneo-scleral  margin  of  animal  and  human  eyes,  and  I 
came  to  the  conclusion  that  these  stripes  are  represented  by 


l6  THE  HUMAN  EYE. 

the  larger  nerve-canals  when  they  are  in  a  state  of  infiltra- 
tion. This  explanation  seems  to  be  the  more  plausible, 
since,  we  know  that  at  the  corneo-scleral  junction,  from  forty 
to  forty-eight  nerves  enter  the  corneal  tissue,  and  our 
operative  wounds  comprise,  from  one-fourth,  to  one-third 
of  the  corneal  periphery.  Moreover,  we  never  see  striped 
keratitis  after  wounds  inflicted  upon  the  centre  of  the  cor- 
nea, where  no  large  nerve-canals  exist. 

Infiltration-keratitis  usually  heals  without  leaving  a  trace, 
sometimes  it  causes  sclerosis,  of  the  involved  parts,  as  above 
stated,  and  in  rare  cases  (except  in  phlyctsenula)  it  leads 
to  purulent  keratitis  with  its  results.  Infiltration-keratitis 
is  furthermore  constantly  found  accompanying  purulent 
keratitis,  and  then  involves  the  tissue  surrounding  the  parts 
suffering  from  the  purulent  form  of  inflammation. 

I  have  never  found  Descemefs  membrane  or  its  endothe- 
lium, altered  in  cases  of  infiltration-keratitis.  This  form  also 
very  rarely  causes  an  inflammation  of  the  tissue  of  the  iris. 

b.  Purulent  Keratitis. 

The  characteristic  feature  of  the  purulent  form  of  kera- 
titis is,  that  the  increase  of  the  cellular  elements  in  the  cor- 
nea is  such,  as  to  destroy  the  corneal  tissue.  This  holds  good 
whether  the  process  involve  only  a  superficial  part  of  the 
corneal  tissue  or  be  deeper  seated,  whether  only  a  part  or  the 
whole  of  the  cornea  be  destroyed. 

We  can  distinguish  three  forms  of  purulent  keratitis,  viz. : 
abscess,  ulcer  and  kerato-malacia. 

c.  Abscess  of  the  Cornea. 

Abscess  of  the  cornea  is  that  form  of  purulent  keratitis 
which  always  takes  its  origin,  in  the  deeper  layers  of  the 
cornea,  and  which  may  remain  altogether  confined  to  them, 
and  never  reach  the  surface  of  this  membrane. 

In  this  form  of  inflammation  we  always  find  a  more  or 
less  roundish,  flattened  part  of  the  corneal  tissue  filled  with 
innumerable  round-cells.  The  pressure  exerted  by  these 
cells  upon  the  stroma  of  the  cornea  leads  to  mortification 
and  fatty  degeneration  of  the  involved  parts,  and  thus  a  pus- 


CORNEA. 


17 


cavity  is  formed.  This  cavity  has  generally  the  shape  of 
a  flattened  globe,  or  is  ovoid,  with  corroded  walls.  Some- 
times trabeculae  may  be  found  springing  from  one  side  of  the 
cavity  and  reaching  to  the  opposite  wall.  The  cavity  itself 
is  perfectly  filled  with  round-cells,  which  often  surround  a 
central  nucleus  of  fatty  (cheesy)  detritus.  The  corneal  tissue 
surrounding  the  abscess  is  in  a  state  of  infiltration,  and  gen- 
erally most  so  on  that  side  of  the  abscess  which  lies  nearest 
the  corneo-scleral  margin. 

In  this  stage  the  process  may  heal,  without  involving 
more  than  the  parts  originally  attacked.  The  healing 
process  always  begins  with  the  formation  of  blood-vessels, 
from  the  corneo-scleral  margin  in  the  way  above  mentioned. 
When  the  detritus  and  the  cells  are  absorbed  the  walls  of 
the  abscess  may  simply  heal  together  or  the  cavity  may 
become  partially  or  totally  filled  up  with  new-formed,  (of 
course  only  translucent)  connective-tissue.  The  blood-ves- 
sels may  become  atrophic  and  disappear  or  remain  persistent. 

As  a  rule,  however,  the  process  does  not  heal  at  this  stage. 
More  cells  immigrate  and  are  formed  by  proliferation  of  the 
old  ones  in  the  original  cavity  and  the  adjoining  tissue,  and 
thus  more  and  more  of  the  parenchyma,  is  destroyed.  It 
may  thus  happen  that  the  destruction  of  the  tissue  reaches 
to  the  outer  surface — that  is,  a  deep  ulcer  may  be  formed. 
In  rare  cases,  when  the  abscess  lies  directly  next  to  Desce- 
mefs  membrane,  this  may  also  be  destroyed,  and  the  abscess 
thus  opens  into  the  anterior  chamber,  which  may  lead  to 
the  formation  of  an  anterior  synechia,  when  the  abscess  lies 
near  the  corneo-scleral  margin.  Moreover,  the  abscess  can 
lead  to  a  total  perforation  of  the  cornea  and  open  at  the 
same  time  upon  the  anterior  and  posterior  surface  of  this 
membrane. 

If  the  abscess  does  not  perforate  either  Bowmafi  s  Id^y^r  or 
Descemefs  membrane,  and  its  contents  are  not  readily  ab- 
sorbed, the  cavity  may  still  be  found  after  all  the  inflam- 
matory symptoms  have  disappeared.  It  may  then  appear  as 
a  cystoid  formation  in  the  cornea.     (See  Fig.  4.) 

Corneal  abscess  is  very  frequently  accompanied  by  the 
formation  of  pus  in  the  anterior  chamber,  which  is  called 


i8 


THE  HUMAN  EYE. 


hypopyon.  There  are  three  ways  in  which  the  formation  of 
hypopyon  may  take  place.  Since  the  corneal  canals,  as  we 
have  seen  above,  communicate  directly  in  the  ligamentum 


Fig.  4.— Cavity  of  an  abscess  in  the  cornea,  after  the  contents  have  been  perfectly  absorbed. 

pectinatum  (through  Fontanels  canals)  with  the  contents  of 
the  anterior  chamber,  the  cells  may  wander  into  the  latter 
through  the  former ;  and  this  is  probably  the  most  common 
way  in  which,  the  formation  of  hypopyon  occurs.  Fur- 
thermore, if  the  abscess  lies  near  Descemefs  membrane  the 
structure  of  this  membrane,  becomes  pathologically  changed. 
It  becomes  dim,  and  often  two  and  three  times  thicker  than 
in  the  normal  condition.  This  change  is  soon  followed  by 
alterations  in  the  endothelial  layer.     Its  cells  grow  larger  and 

begin     to     proliferate, 


and  the  new-formed 
more  or  less  roundish 
cells  lie  at  first  in  lit- 
tle clusters  on  the 
posterior  surface  of 
Descemei' s   membrane. 

Fig.  5. — Shows  proliferation  of  the  endothelium  of  Des-  Later  Oil  thev    beCOmC 
cemefs   membrane,   in  a   case  of   corneal    abscess  1       r   11 

with  hypopyon.  detachcd    and    fall   to 

the  bottom  of  the  anterior  chamber.  (See  Fig.  5).  If  the 
abscess  lies  near  the  corneo-scleral  margin,  the  iris  and  ciliary 
body  frequently  become  inflamed  also,  and  the  inflammation 
of  these  parts  is  then  the  third  means  of  the  formation  of  pus 


CORNEA. 


19 


in  the  anterior  chamber.     Hypopyon  thus  formed  contains, 
as  a  rule,  some  fibrinous  matter. 

If  the  abscess  leads  to  the  formation  of  an  ulcer  or  to 
total  perforation  of  the  cornea,  it  is  the  final  cause  of  more 
serious  results,  of  which  we  shall  have  to  speak  later  on. 

b.   Ulcer  of  the  Cornea. 

Every  loss  of  substance  of  the  cornea,  caused  by  purulent 
inflammation,  and  reaching  to  the  surface,  is  an  ulcer,  whether 
the  pathological  process  began  originally  on  the  surface  itself, 
or  involved  at  first  the  deeper  layers  only,  and  attacked  the 
superficial  ones  at  a  later  period. 

The  process  of  ulceration  begins,  as  a  rule,  from  the  sur- 
face of  the  cornea,  although,  as  just  mentioned,  it  may  also 
begin  in  the  deeper  layers.     We  mostly  find  at  first  an  infil- 


FiG.  6. — Ulcer  ofthe  cornea ;  its  ground  and  walls  lined  with  round-cells,  the  surrounding 
epithelium  proliferating. 

tration  of  the  lamellae  lying  next  to  Bowman'' s  layer.  The 
number  of  cells  is  rapidly  increased,  and  Bowman  s  layer  as 
well  as  the  epithelium  are  raised,  and  the  latter  begins  to 
decay.  The  destruction  is  generally  first  noticed  in  its  most 
superficial  layers,  and  only  gradually  takes  up  the  remaining 
ones.  Meanwhile  the  attacked  lamellse  and  finally  Bowman's 
layer  also  become  destroyed,  a4;id  thus  an  ulcer  is  formed. 
Its  base  is  covered  with  pus,  its  walls  are  ragged,  and  the 
adjoining  corneal  tissue  is  filled  with  a  large  number  of  round 
cells,  which   decrease  nearer  the   periphery  of  the  cornea. 


20  TTTE  HUMAN  E  YE. 

The  epithelium  surrounding  the  ulcer  is  also  in  a  pathologi- 
cal condition.  It  becomes  very  much  thickened  in  conse- 
quence of  the  proliferation  of  its  cells,  especially  in  its  middle 
layers.  The  new-formed  cells  are  nearly  all  serrated  ones. 
In  some  specimens  I  found  the  proliferation  going  on  also  in 
the  flattened  (superficial)  cells  and  in  the  basal  layer.  (See 
Fig.  6.) 

The  conditions  are  entirely  the  same  when  the  ulcer  is 
the  result  of  a  previous  abscess  of  the  cornea. 

In  this  stage  the  process  may  stop  and  the  ulcer  heal. 
If  it  progresses,  the  parts  surrounding  it  become  more  and 
more  infiltrated  and  also  destroyed,  in  the  manner  described 
above. 

A  strange  change  takes  place  in  the  direction  of  the 
lamellae,  which  form  the  base  and  walls  of  the  ulcer.  They 
become  bent  towards  the  surface  at  an  angle  of  about  forty- 
five  degrees.  This  is  probably  the  result  of  mechanical  in- 
fluences. 

If  the  ulcer  no  longer  progresses,  its  bottom  cleanses 
itself  and  its  margins  lose  their  ragged  appearance.  At  the 
same  time,  if  the  ulcer  is  not  entirely  superficial,  a  new-for- 
mation of  blood-vessels  from  the  cornea-scleral  margin  takes 
place,  as  has  been  previously  described.  It  seems  that  in 
these  cases  new  vessels  lie,  as  a  rule,  in  the  more  superficial 
layers  of  the  cornea.  Otherwise  they  differ  in  no  way  from 
the  new-formed  blood-vessels  we  found  during  the  healing 
process  of  an  abscess. 

The  third  stage  of  the  disease,  the  reparation  of  the  loss 
of  substance,  is  ushered  in  by  a  marked  proliferation  of  the 
epithelium,  which  sometimes  very  rapidly  grows  over  the 
whole  area  of  the  ulcer.  I  am  not  certain  whether  one 
special  layer  of  the  epithelium  is  the  active  one  in  this  pro- 
cess, but  it  seems  to  me  that  all  the  layers  take  an  active 
part  in  it.  The  new-formed  epithelial  cells  vary  greatly  in 
shape  and  size;  they  are  mostly  roundish,  sometimes  cylinder 
and  spindle-shaped.  , 

As  soon  as  the  epithelium  begins  to  grow,  a  new  and  at 
first  very  delicate  connective-tissue,  which  is  filled  with  a 
great  number  of  cells,  is  formed  upon  the  ulcer.     The  epi- 


CORNEA. 


21 


thelium,  however,  always  covers  the  loss  of  substance  before 
the  new-formed  tissue  has  reached  the  level  of  the  surface  of 
the  cornea. 

This  new-formed  tissue  afterwards  becomes  much  denser 
and  tougher.  Since  Bowman  s  layer  is  never  regenerated  as 
such,  the  epithelium  is  no  longer  supported  in  the  normal 
way,  and  grows  into  the  new-formed  connective-tissue  in  the 
shape  of  papillae  of  different  size.  (See  Fig.  7.)  The  margins 
of  Bowmajts  layer  around  the  original  loss  of  substance  are 
generally  bent  inward,  and  the  new-formed  tissue  lies  often 
on  their  outer  surface,  without,  however,  producing  a  thick- 
ening of  the  cornea.  When  the  new-formed  tissue  is  per- 
fectly dense  it  appears  somewhat  lamellar,  like   the  normal 


Fig.  7. — Healed  corneal  ulcer.    The  loss  of  substance  filled  with  new-formed  connective- 
tissue  into  which  the  epithelial  layer  sends  papillary  offsets. 

corneal  tissue.  The  lamellse  are,  however,  much  smaller  than 
the  normal  ones,  and  are  not  arranged  as  regularly  as  these, 
but  intersect  each  other  at  obtuse  angles.  The  fascicles 
which  form  the  new  lamellae  are  also  much  smaller,  and  show, 
even  a  long  time  after  the  healing  process  has  been  com- 
pleted, a  much  larger  amount  of  cellular  elements  than  the 
normal  surrounding  corneal  tissue.  The  new-formed  blood- 
vessels disappear,  as  a  rule,  or  they  may  remain  persistent. 

The  new-formed  tissue  is,  as  is  well  known,  only  trans- 
lucent, and,  although  it  generally  clears  up  somewhat  when 
the  process  of  reparation  is  over,  it  never  becomes  trans- 
parent. 

If  the  progress  of  the  ulcer  does  not  stop  in  the  way  we 


22  THE  HUMAN  E  YE. 

just  described,  it  destroys  more  and  more  of  the  corneal  tissue, 
and  finally  leads  to  perforation  of  Descemefs  membrane. 
Before  this  membrane  is  perforated,  however,  it  is  generally 
pressed  forward  and  protrudes  towards  the  surface  of  the 
cornea,  a  condition  which  has  been  called  myocephalon  or 
keratocele.  This  protrusion  of  Descemefs  membrane  may  be 
caused  by  the  normal  intra-ocular  pressure ;  but  it  is,  how- 
ever, usually  increased. 

If  Descemefs  membrane  be  thus  perforated,  the  aqueous 
humor  flows  off,  and  the  iris  may  become  either  simply  at- 
tached to  the  cornea  or  prolapse  into  the  wound-canal,  which 
conditions  we  shall  have  to  describe  more  fully  later  on. 

With  the  microscope  we  are  always  able  to  detect  a 
former  ulcer  by  the  following  conditions  :  the  irregular  thick- 
ness of  the  epithelial  layer,  the  partial  absence  of  BoivmarCs 
layer,  and  the  translucent,  irregularly  lamellated  scar-tissue, 
with  its  abnormal  number  of  cellular  elements. 

Sometimes  we  find  srhall  particles  of  metallic  substances 
in  this  scar-tissue,  which  have  been  brought  there  by  the  use 
of  metallic  collyriums.  Saeinisch  also  found  cavities  filled 
with  colloid  substance. 

xA.ll  the  different  forms  of  ulcers,  as  distinguished  by  cHni- 
cists,  show  these  same  histological  conditions.  The  parasites, 
which  in  recent  times  have  been  considered  of  great  impor- 
tance in  the  formation  of  every  disease,  have,  of  course,  also 
been  found  in  the  cornea.  I  have  never  been  able  to  con- 
sider them  as  the  important  agents  they  are  thought  to  be 
by  others,  at  least  in  diseases  of  the  eye. 

y.  Keratomalacia. 

It  is  the  characteristic  feature  of  keratomalacia,  that  the 
deleterious  new-formation  of  cells  concerns  and  destroys  the 
whole  of  the  corneal  tissue. 

In  all  other  points  this  process  is  the  same  as  has  just 
been  described.  The  whole  of  the  corneal  tissue  becomes 
mortified  and  is  thrown  off.  The  ensuing  loss  of  substance 
is  repaired  through  tissue  growing  from  the  surrounding  con- 
junctiva and  episclera.  When  the  loss  is  thus  perfectly  re- 
paired by  the  newly-formed  connective-tissue,  we  find  what 


CORNEA. 


23 


has  been  styled  by  clinicists  phthisis  anterior,  namely,  a 
grayish,  translucent  connective-tissue  in  the  place  of  the 
cornea,  which  is  either  flat  or,  as  often  happens  in  a  later  stage 
through  morbid  changes  in  the  interior  of  the  eyeball,  drawn 
inward. 

Although  it  is  not  out  of  place  to  consider  abscess,  ulcer 
and  keratomalacia  as  three  different  and  distinct  types  of 
inflammation  of  the  corneal  tissue,  I  will  here  again  state 
that  from  an  abscess  an  ulcer  may  originate,  and  that  kerato- 
malacia may  as  well  be  the  result  of  an  abscess  as  of  an  ulcer. 

In  all  of  these  inflammatory  processes  of  the  corneal  tis- 
sue the  conjunctiva  and  episclera  are  more  or  less  altered. 
The  purulent  form  of  keratitis  often  cause  inflammatory  pro- 
cesses in  the  tissue  of  the  iris  sometimes  of  the  whole  uveal 
tract,  and  in  a  small  number  of  cases  causes  panophthalmitis. 


The  Results  of  Keratitis. 

a.  Formation  of  Scars  and  Panniis. 

Losses  of  substance,  which  concern  only  the  epithelial 
layer,  and  leave  the  substantia  propria  of  the  cornea  intact, 
usually  heal,  without  leaving  a  trace.  If,  however,  the 
smallest  particle  of  the  corneal  tissue  itself  is  destroyed, 
scar-tissue  is  formed  to  repair  the  loss.  This  newly-formed 
tissue  is  only  translucent,  and  according  to  the  degree  in 
which  it  lacks  transparency,  we  call  it  clinically  nebecula, 
macula  or  leuconia  of  the  cornea.  It  is  evident  from  this 
that  as  a  rule  only  the  purulent  forms  of  keratitis  will  pro- 
duce persistent  alterations  in  the  corneal  tissue. 

As  above  stated  infiltration  keratitis  may  lead  to  sclerosis 
of  the  cornea,  and  this  is  mostly  the  case  when  infiltra- 
tion lies  near  to  or  at  the  corneo-scleral  margin.  This 
sclerosis  has  erroneously  been  called  interstitial  keratitis.  As 
already  stated,  the  sclerosis  is  caused  by  the  new-formation  of 
connective-tissue  between  the  normal  lamellae  of  the  sub- 
stantia propria  of  the  cornea,  which  obliterates  the  corneal 
canals,   which   by   retracting   reduces   the  quantity  of  fluid 


24 


THE  HUMAN  E  YE. 


in  the  tissue  of  the  lamellae  and  produces  atrophy.  This 
new-formed  tissue  is  formed  from  the  fixed  and  wandering 
corneal  cells,  and  the  sclerosed  tissue,  furthermore,  is  dis- 
tinguished from  scar-tissue  by  its  want  of  cellular  elements. 

Nebecula,  macula  and  leucoma  are  clinical  names  for 
the  same  histological  condition,  namely,  scar-formation  in 
the  tissue  of  the  cornea.  The  way  in  which  these  scars  are 
formed  has  been  described  above  under  the  head  of  Purulent 
Keratitis.  Besides  the  cavities  filled  with  colloid  and  metal- 
lic deposits  which  were  mentioned  at  the  same  place,  deposits 
of  lime  are  not  infrequently  found  in  such  scars,  and  they 
consist  of  granules  which  are  round  or  shell-like.    (See  Fig.  8.) 


Fig.  8.— Deposits  of  lime  in  the  cornea  of  a  staphylomatous  eye. 

They  lie  mostly  in  the  anterior  parts  of  the  cornea,  directly 
under  the  epithelium,  and  I  think  they  begin  in  the  blood- 
vessels, whose  ramifications  are  often  beautifully  shown  by 
these  deposits.  It  is  not  improbable  that  ossification  of  the 
cornea  described  by  Stellwag  was  in  reality  nothing  but  such 
deposits  of  lime. 

In  phthisis  anterior  and  large  scars  of  the  cornea  the  epi- 
thelium is  often  very  much  altered.  It  is  found  mostly  horny 
or  in  a  state  of  colloid  metamorphosis. 

Here  we  should  mention,  what  is  called  a  facette.  Al- 
though I  never  had  the  occasion  to  examine  a  facette  mi- 
croscopically, it  may  be  deduced  from  clinical  observation 
that  in  such  cases  the  loss  of  substance  is  covered  by  epithe- 
lium only,  without  the  new-formation  of  connective-tissue. 
The  peculiarity  of  a  facette  is  therefore  that  the  loss  of  sub- 


CORNEA. 


25 


Stance  is  in  reality  never  filled  up  again,  although  covered 
with  epithelium,  and  this  is  why  it  hardly  ever  shows  any 
dimness. 

The  formation  of  what  is  called  pannus  of  the  cornea  has 
been  spoken  of  before.  I  have  here  only  to  mention  the 
conditions  of  persisting  pannus.  In  pannous  corneae  we 
find  large  blood-vessels  with  a  well-developed  adventitia 
and  capillary  blood-vessels.  It  is  always  easy  to  trace  their 
origin  back  to  the  vessels  of  the  corneo-scleral  margin. 
Where  they  lie  in  normal  corneal  tissue  they  appear  sur- 
rounded by  a  new-formed  tissue,  which  when  young  is  fine 
and  cellular,  and  later  on  becomes  tough  and  bare  of  cells. 
This  tissue  causes  the  dimness  of  the  cornea  which  always 
accompanies  the  pannus.  Small  hemorrhages  are  not  rare 
in  this  tissue,  and  may  be  found  also  in  vascular  scar-tissue. 

As  has  been  stated  above.  Bowman's  layer,  when  once 
destroyed,  is  never  regenerated ;  the  same  holds  good  for 
Descemef s  membrane.  The  latter  is,  however,  never  de- 
stroyed to  the  same  extent  as  the  former,  and,  if  the 
cornea  has  been  perforated  upon  its  outer  or  inner  surface, 
Descemefs  membrane,  is  always  found  drawn  into  the  canal 
of  the  perforation,  and  adhere  it  to  its  walls. 

b.  Anterior  Synechicz, 

Anterior  synechias  are  very  frequently  the  result  of  puru- 
lent keratitis,  when  the  latter  has  led  to  perforation.  The 
name  anterior  synechise  is  usually  applied  only  to  the  adhe- 
sions of  the  iris  to  the  cornea  ;  there  are,  however,  as  well 
anterior  synechiae  of  the  crystalline  lens,  or,  if  the  lens  is 
wanting,  of  the  vitreous  body. 

In  anterior  synechia  of  the  iris,  this  membrane  may 
simply  adhere  with  its  anterior  surface  to  the  posterior  sur- 
face of  the  cornea,  or  the  iris  may  have  been  drawn  more  or 
less  far  into  the  canal  of  the  perforation,  and  having  grown 
together  with  the  corneal  tissue  may  there  be  incarcerated. 
If  the  anterior  surface  of  the  iris  only  is  adherent  to  the  pos- 
terior surface  of  the  cornea,  this  adhesion  need  not  necessarily 
have   taken    place   at  the  site  of  the  perforation,  but  may 


26 


THE  HUMAN  EYE. 


also  He  in  the  neighborhood  of  the  latter.  The  endothelium 
of  Descemefs  membrane  and  the  anterior  surface  of  the  iris 
are  always  wanting- in  these  places,  and  is  replaced  by  a 
small  layer  of  tissue,  consisting  of  long  delicate  spindle- 
shaped  cells,  which  are  transformed  endothelial  cells.  That 
this  is  really  the  case  is  readily  proven  in  specimens  where 
the  adhesion  has  only  partly  been  accomplished.  The 
endothelial  cells  then  are  seen  to  be  partly  enlarged,  or  to 
have  one  or  two   offsets,  while  others  are  already  spindle- 


FiG.  q.— A  nterior  synechia  between  cornea  and  iris.  The  endothelium  of  Descemet's  mem- 
brane forming  a  layer  of  spindle-shaped  cells  around  the  place  where  iris  and  cornea 
are  united. 

shaped.  Sometimes  these  endothelial  cells  are  also  found  to 
undergo  a  regressive  metamorphosis,  and  colloid  degenera- 
tion is  comparatively  the  most  frequent  one. 

If  the  iris  has  been  drawn  into  the  canal  of  the  perfora- 
tion and  there  become  adherent,  it  is  after  some  time  impos- 
sible to  make  out  the  exact  line  where  the  tissue  of  the  iris 
is  united  to  that  of  the  cornea,  as  they  coalesce  perfectly. 
(See  Fig.  9.)  The  pigmented  cells  of  the  parenchyma  of  the 
iris  and  the  blood-vessels  of  the  latter  grow  into  the  cornea, 


CORNEA. 


27 


and  minute  particles  of  pigment,  freed  by  the  destruction  of 
tlie  cells,  are  seen  to  be  thrown  some  distance  into  the  neigh- 
boring corneal  tissue,  and  there  remain  stationary.  In  the 
beginning  of  this  process  cornea  and  iris  are  full  of  lymphatic 
cells,  which  later  on  disappear. 

Desceniefs  membrane  is  in  these  cases  generally  drawn 
with  the  iris  into  the  canal  of  the  perforation,  and  sometimes 
its  ends  are  bent  inward  upon  the  iris.  In  the  first  case  the 
endothelial  cells  help  in  the  formation  of  the  scar-tissue,  and 
can  no  longer  be  distinguished.  In  the  second  case  the  en- 
dothelial cells  are  found  transformed  into  spindle-cells,  as 
described  above,  and  they  form  a  small  layer  of  delicate 
tissue  in  the  angles,  where  Descemefs  membrane  is  bent 
backward  upon  the  iris  and  upon  the  latter. 

The  two  different  kinds  of  anterior  synechia  of  the  iris,  viz., 
simple  adhesion  and  incarceration,  are  found  in  all  parts  of  the 
cornea.     Their  histological  conditions  are  always  the  same. 

Anterior  synechiae  between  the  crystalline  lens  and  cornea 
are  very  much  rarer.  They  are  generally  combined  with  an- 
terior synechia  of  the  iris,  or  in  rare  cases  seen  without  the 
former.  They  are  furthermore  mostly  found  in  eyes  suffering 
from  staphyloma  of  the  cornea.  In  all  of  the  cases  which  I 
had  occasion  to  examine,  the  crystalline  lens  was  cataractous. 
Sometimes  the  anterior  capsule  of  the  crystalline  lens  was 
simply  adherent  to  the  inner  orifice  of  the  canal  of  a  perfora- 
tion, without  being  ruptured ;  sometimes  the  capsule  was 
ruptured,  and  new-formed  connective-tissue  had  grown  into 
it.  O.  Becker  states  that  in  cases  of  anterior  polar  cataract, 
we  have  a  right  to  diagnose  an  intra-uterine  perforation  of 
the  cornea  with  anterior  synechia  of  the  crystalline  lens. 

Although  it  is  probable  that  anterior  synechiae  between 
the  vitreous  body  and  the  cornea,  especially  in  eyes  from 
which  the  crystalline  lens  has  been  removed  by  an  operation 
or  an  injury,  are  more  frequent  than  we  know  of,  I  only  once 
had  an  opportunity  to  examine  such  a  specimen.  (See 
Fig.  10.) 

The  specimen  is  taken  from  an  eye  enucleated  on  account 
of  ciliary  staphyloma.  The  following  are  the  histoolgical 
conditions. 


28  THE  HUMAN  EYE. 

Nearly  in  the  centre  of  the  cornea  the  above  described 
results  of  ulceration  and  perforation  are  to  be  seen.  The 
crystalline  lens  is  wanting.     The  vitreous  body  is  healed  in 


Fig.  io. — Anterior  synechia  between  cornea  and  vitreous  body. 

the  form  of  a  cone  into  the  scar-tissue  of  the  cornea.  It  is 
here  transformed  into  connective-tissue  and  perfectly  coa- 
lesces with  the  corneal  scar.  The  wound-lips  of  Descejnefs 
membrane  lie  upon  the  iris,  and  can  be  traced  farther  back- 
ward than  would  be  possible  if  they  had  simply  been  bent 
backward.  A  new-formation  of  vitreous  substance  must 
therefore  have  taken  place.  The  surface  of  the  conical  pro- 
lapse of  the  vitreous  body  has  a  network  of  delicate  fibrills, 
in  the  meshes  of  which  a  number  of  oval  and  bean-like  cells 
with  an  oval  and  finely  granulated  nucleus  are  embedded. 
The  cells  of  this  network  pass  gradually  over  into  the  en- 
dothelial cells  oi  Descemefs  membrane,  and  are  probably  de- 
rived from  them.  The  posterior  part  of  the  vitreous  body  is 
liquefied.  (Similar  pictures  are  drawn,  {o\  instance,  in  Iwan- 
off's  experiments  on  the  detachment  of  the  vitreous  body.) 

Anterior  synechiae  of  the  iris  and  vitreous  body  are  of 
course  very  apt  to  cause  chronic  inflammation  of  the  in- 
volved parts,  which  are  continuously  dragged  upon  in  the  act 
of  accommodation.  The  anterior  synechiae  of  the  crystalline 
lens  can  have  the  same  effect  by  continuous  pressure  upon 
the  iris.  These  conditions  are  therefore  very  frequently  the 
origin  of  the  perfect  destruction  of  the  so  diseased  eye,  and 
of  sympathetic  affection  of  its  fellow. 

Anterior  synechiae  of  the  iris  are  moreover  sometimes  the 


CORNEA.  29 

origin  of  the  so-called  cysts  of  the  iris,  which  will  be  treated 
of  later  on. 

c.  Prolapsus  iridis  and  granuloma  iridis  traumaticum. 
These  will  be  spoken  of  in  Chapter  IV. 

d.  Keratoconus  e  cicatrice  and  staphyloma  cornece. 

Since  purulent  keratitis,  as  has  been  above  stated,  mostly 
produces  irritation  or  even  inflammation  of  the  uveal  tract, 
it  is  often  combined  with  an  increase  of  intra-ocular  pres- 
sure. The  new-formed  scar-tissue  is  therefore  (the  more  so 
as  the  supporting  layer  of  Bowman  is  wanting)  frequently  not 
strong  enough  to  retain  the  normal  curvature  of  the  cornea. 

If  the  scar  lies  in  or  very  near  the  centre  of  the  cornea, 
and  there  is  no  anterior  synechia,  the  intra-ocular  pressure 
may  stretch  the  tissues  more  symmetrically,  and  thus  pro- 
duce a  conical  cornea  (keratoconus.)  (Keratoconus,  which 
is  sometimes  seen  as  an  humory  malformation  and  without  a 
scar  of  the  cornea,  does  not  belong  here.)  We  find  in  these 
cases  at  a  later  period  the  radius  of  the  whole  cornea  consid- 
erably shortened  and  the  cornea,  especially  the  central  scar 
and  Descemefs  membrane,  which  is  mostly  unruptured,  very 
much  thinned.  If  the  keratoconus  is  so  large  that  the  lids 
can  no  longer  perfectly  cover  its  apex,  the  epithelial  layer 
upon  it  is  often  transformed  into  horny  scales. 

This  conical  stretching  of  the  cornea  may  become  sta- 
tionary at  any  time ;  it  can,  however,  also  progress  until 
it  leads  to  a  spontaneous  rupture  of  the  eye  and  subsequent 
phthisis,  with  its  dangerous  consequences. 

If  the  cornea  has  been  perforated  and  a  partial  or  total 
anterior  synechia  of  the  iris  or  a  synechia  between  iris,  crys- 
talline lens  and  cornea  has  been  the  result,  the  intra-ocular 
pressure  frequently  causes  the  formation  of  a  partial  or  total 
staphyloma  of  the  cornea.  The  name  staphyloma  of  the 
cornea  can  therefore  only  be  applied  to  those  cases  where 
the  iris  at  least  is  adherent  to  the  stretched  and  bulging  scar- 
tissue  of  the  cornea — that  is,  where  an  adherent  leucoma 
yields  to  the  intra-ocular  pressure.  We  find,  therefore,  in 
these  cases  not  only  the  corneal  scar,  but  also  the  iris,  unduly 


30 


THE  HUMAN  EYE. 


Stretched.  The  latter  membrane  often  becomes  so  atrophic 
that  it  is  represented  only  by  a  thin  layer  of  pigment  upon 
the  posterior  surface  of  the  cornea.  The  cornea  is  mostly 
attenuated  in  the  same  way  as  into  keratoconus  and  atrophic ; 
in  rare  cases,  however,  hypertrophic,  and  even  sometimes  to 
a  high  degree.    (See  Fig.  ii.)    Manz  stated  that  he  found 


Fig.  II. — Staphyloma  of  the  cornea,  with  hypertrophy  of  the  latter. 

in  cases  of  staphyloma  of  the  cornea  an  abnormally  large 
number  of  serrated  epithelial  cells.  From  what  has  been 
stated  above,  it  is  evident  that  this  condition  is  not  peculiar 
to  staphyloma  only.  If  the  staphyloma  is  so  large  that  the 
lids  can  no  longer  cover  it,  its  epithelial  layer  is  often  found 
horny  or  in  colloid  metamophosis.  Deposits  of  phosphate 
of  lime  are  not  very  rare  in  such  staphylomatous  corneae. 

e.  Pterygitan. 

The  formation  of  pterygium  of  the  conjunctiva  may  be 
caused  by  a  marginal  ulcer  of  the  cornea.  This  happens  in 
the  following  way.  The  marginal  ulcer  causes  infiltration 
and  swelling  of  the  adjacent  parts  of  the  conjunctiva,  a  fold 
of  which  comes  into  contact  with  the  corneal  ulcer,  and  grad- 
ually becomes  adherent  to  its  walls  and  bottom.  That  this 
may  be  really  the  case  was  proven  in  a  case  which  I  have 
described  elsewhere,  by  the  fact  that  Bowman  s  layer  was 
severed  from  the  periphery  of  the  corneal  tissue  and  bent 
backward   upon  itself.     Furthermore,  I  found  the  conjunc- 


CORNEA. 


31 


tival  epithelium  incarcerated  between  the  conjunctival  tissue 
of  the  pterygium  and  the  ground  of  the  corneal  ulcer,  and  in  a 
state  of  colloid  degeneration.  The  whole  of  the  tissue  of  the 
pterygium,  which  grows  like  a  wedge  into  the  corneal  tissue, 
is  merely  unaltered  conjunctiva,  and  we  shall  therefore  have 
more  to  say  upon  this  subject  in  the  chapter  treating  on  this 
membrane,  the  more  so,  since  pterygium  is  not  always  caused 
by  a  marginal  ulcer  of  the  cornea.     (See  Figs.  12  and  13.) 


Fig,  12  —Section  through  a  pterygium  in  a  meridional  direction.    Pt.  Pterygium.    A.  Cor- 
neal lamellx  raised  by  the  pterygium.  B.  Bowman's  layer.  C.  Normal  corneal  lamellae. 

B.  Injuries  to  the  Cornea,  their  Mode  of  Healing 

AND   THEIR   RESULTS. 

a.  Injuries  without  the  retention  of  a  foreign  body. 

Injuries  of  the  cornea  which  entail  a  loss  of  substance  of 
this  membrane,  always  lead  to  the  formation  of  an  ulcer,  if 
ever  so  small,  and  heal  in  the  same  manner.  They  fall  there- 
fore under  the  head  of  purulent  keratitis.  They  are  rents  or 
scratches,  and  such  injuries  by  which  a  segment  is  cut  off  from 
the  surface  of  the  cornea.     The  conditions  are  different  when 


32 


THE  HUMAN  E  YE. 


the  cut  is  linear  or  an  instrument  has  been  thrust  through 
the  cornea  and  only  severed  the  continuity  of  the  tissue, 
without  causing  a  loss  of  substance. 

Let  us  first  examine  those  conditions  which  are  found  when 
an  uncomplicated  cut  has  been  inflicted  upon  the  cornea.  This 

ft  .. 


S 

Fig.  13. — Equatorial  section  through  a  pterygium.  Pt.  Pterygium.  S.  Sclerotic  (corneo- 
scleral margin).  E.  Encapsuled  conjunctival  epithelium  undergoing  regressive  meta- 
morphoses. 

cut  may  involve  only  a  part  of  the  cornea  or  perforate  its  whole 
thickness,  the  healing  process  will  be  essentially  the  same. 

As  soon  as  three  hours  after  the  cornea  has  thus  been  cut, 
the  lips  of  the  wound  may  be  found  infiltrated  with  round- 
cells  (cl.  Infiltration  of  cornea.)  These  cells  can  only  be  immi- 
grated ones,  and  cannot  as  yet  be  considered  as  resulting  from 
a  proliferation  of  the  fixed  corneal  cells.  Very  soon  after- 
wards (in  eight  or  ten  hours)  a  fibrinous  substance  is  exuded 
into  the  canal  of  the  wound,  which  is  soon  also  invaded  by 
the  round-cells.  The  epithelium  margin  of  Bozvman  s  layer 
and  they  very  soon  after  the  injury  has  been  inflicted,  appear 
bent  inward,  and  two  or  three  days  afterward  the  epithelial 
cells  are  seen  to  proliferate  into  the  wound-canal.  It  seems 
that  the  new  epithelial  cells  take  their  origin  from  the 
basal  layer  and  the  serrated  cells ;  they  lack,  however,  the 


CORNEA. 


33 


typical  shape.  (See  Fig.  14.)  While  this  proliferation  of 
the  epithelial  cells  takes  place,  the  fibrinous  exudation 
in  the  wound-canal  is  transformed  into  connective-tissue, 
which  at  first  is  very  delicate  and  filled  with  Cells,  and  later 
on  becomes  denser  and  denser,  and  loses  the  numerous  cells 


Fig.  14. — A  healing  corneal  wound  four  days  after  it  was  inflicted. 

accordingly.  At  this  period  of  the  healing  process  the 
epithelium  generally  fills  the  outer  third  of  the  wound- 
canal.  If  the  wound  has  pierced  the  whole  thickness  of  the 
cornea,  the  wound-lips  o{  Descemef  s  membrane  are,  as  a  rule, 
at  first  projecting  into  the  anterior  chamber  in  consequence 
of  the  pressure  exerted  upon  them  by  the  fibrinous  ex- 
udation. This  condition,  although  declared  to  be  final  by 
Becker,  is,  however,  not  stationary.  As  soon  as  the  new- 
formed  scar-tissue  begins  to  shrink,  the  lips  of  the  wound  of 
Descemefs  membrane  are  dragged  into  the  wound-canal. 
This  condition  remains  stationary,  and  the  wound-lips  of  this 
membrane  are  never  reunited.  The  endothelial  cells  cover- 
ing them  begin  also  very  frequently  to  proliferate,  and  then 
take  part  in  the  formation  of  the  scar-tissue. 

When  the  scar-tissue  thus  formed  becomes  dense  and 
consolidated,  the  epithelial  cells  which  had  entered  the 
wound- canal  partly  disappear  again,  and  we  then  find  only  a 
small  offset  dipping  through  Bowman  s  membrane  into  the 
corneal  parenchyma  in  the  shape  of  an  epithelial  papilla. 
Sometimes  the  proliferation  of  epithelial  cells  is  so  considera- 


34 


THE  HUMAN  EYE. 


ble  that  secondary  cylinders  are  seen  to  start  from  this  pri- 
mary papilla  and  grow  into  the  adjacent  parts  of  the  corneal 
tissue,  just  as  we  shall  later  on  find  it  when  we  treat  of  the 
epitheliomatous  growths  of  the  cornea.  These  secondary 
cylinders,  however,  never  remain  stationary,  and  have  always 
disappeared  when  the  scar  is  perfectly  consolidated. 

Every  uncomplicated  wound  of  the  cornea  (which  does 
not  cause  the  formation  of  an  ulcer)  heals  in  the  way  just  de- 
scribed, and  the  histological  conditions  are  so  typical  that  we 
can  never  err  in  the  diagnosis. 

From  these  facts,  gleaned  from  the  study  of  the  healing 
process  of  corneal  wounds,  it  is  quite  possible  to  explain  the 
way  in  which  a  corneal  fistula  may  be  formed.  I  have  never 
had  the  occasion  to  examine  such  a  fistula.  But,  if  we  as- 
sume that  the  epithelium  may  grow  through  the  whole  of 
the  wound-canal,  or  that  the  fibrinous  exudation  is  by  some 
cause  or  other  not  transformed  into  connective-tissue,  we 
easily  understand  that  the  intra-ocular  pressure,  especially 
if  it  is  somewhat  increased,  can  re-open  the  canal.  Corneal 
fistulae  are,  as  a  rule,  temporarily  closed,  until  the  anterior 
chamber  is  refilled  and  the  intra-ocular  pressure  reestablished, 
when  the  fistule  is  again  opened.  It  is  true,  a  corneal  fistula 
is  very  rarely,  if  ever,  observed  after  a  wound,  but  is  generally 
the  result  of  an  ulcer  which  has  led  to  perforation  of  the  cor- 
nea. The  ulcers  in  these  cases  are,  however,  as  a  rule,  so 
small  that  their  healing  process  is  probably  not  greatly  at 
variance  with  the  one  after  a  perforating  wound. 

Wounds  which  lie  in  the  corneo-scleral  border  heal  some- 
what differently,  especially  when  accompanied  by  prolapse 
of  the  iris.  In  the  latter  case  the  conditions  greatly  or  alto- 
gether resemble  those  found  after  purulent  keratitis  with  sub- 
sequent anterior  synechia  of  the  iris,  and  need  not  be  dwelled 
upon  again  here. 

Corneo-scleral  wounds  generally  gape  more  than  those  in 
the  centre  do,  and  therefore  the  fibrinous  exudation  found 
between  the  wound-lips  is  generally  larger,  and  the  healing 
process  is  therefore  more  protracted.  The  fibrine,  more- 
over, generally  protudes  over  the  outer  surface  of  the  cornea, 
and  the  epithelium  here  rarely  grows  into  the  wound-canal. 


CORNEA. 


35 


The  epithelial  cover  for  the  new-formed  scar-tissue  is  two- 
thirds  derived  from  the  conjunctival  epithelium.  Since  these 
wounds  lie  close  to,  or  even  sever  the  marginal  blood-vessels 
of  the  cornea,  new  blood-vessels  are,  as  a  rule,  formed  during 
the  healing  process.  Striped  keratitis,  which  mostly  accom- 
panies the  healing  of  such  corneo-scleral  wounds,  has  been 
more  extensively  treated  of  under  the  head  of  Infiltration- 
Keratitis. 

Corneo-scleral  wounds  are  most  frequently  caused  by 
operations,  especially  iridectomy.  When  examining  such 
eyes  we  find,  nearly  invariably,  some  part  of  the  iris  incar- 
cerated in  the  wound.  The  cause  of  this  fact  is  certainly 
that  the  stump  of  the  iris  is  comparatively  too  long  or  the 
corneo-scleral  wound  lies  too  peripheric  in  comparison  with 
the  length  of  the  iris-stump.  (See  Fig.  15.)  If  the  stump 
of  the  iris,  for  instance,  were  as  long 
as  S  in  Fig.  15,  and  the  corneo-scleral 
section  lay  in  A,  an  incarceration  of  the 
former  in  the  latter  would  be  nearly 
impossible,  while  if  the  section  lay 
in  B,  the  stump  could  very  easily 
be  thrown  between  the  inner  lips  of 
the  section  and  there  become  retained. 

In  other  cases  not  the  stump  but 
neighboring  parts  of  the  iris  become 
incarcerated.  It  will  be  hardly  possi- 
ble to  evade  this  ;  but  it  might  be  ren- 
dered less  frequent  by  making  the 
corneal   section   no   larger    than    the  F'«-  's.-stump  of  iris  after  in- 

*-"  dectomy.    Mode  in  whicti  it  be- 

COloboma  of  the  iris.  comes  entangled  in  the  corneal 

These  incarcerations  of  the  iris  are 
frequently  the  cause  of  the  formation  of  a  kind  of  partial 
staphyloma,  which  is  generally  described  as  cystoid  or  ectatic 
scar. 

In  all  of  these  cases  we  find  pigment-molecules  in  the 
corneal  canals  adjoining  the  section.  Sometimes  also  in- 
tact living  pigmented  cells  from  the  iris  wander  into  the 
cornea,  and  are  there  retained.  These  may,  later  on,  pro- 
liferate and  lead  to  the  formation  of  a  corneal  cyst,  which 


36 


THE  HUMAN  E  YE. 


is  lined  by  an  irregular  layer  of  pigmented  endothelial  cells 
and  filled  with  a  serum-like  fluid.     (Fig  i6.) 

It  has  been  stated  above  that   complicated  corneal  and 
corneo-scleral  wounds  may  produce  the  same  effects  as  pur- 


FiG.  i6. — Pigmented  cystoid  formation  in  the  cornea. 

ulent  keratitis.  We  must  therefore  also  enumerate  them 
among  the  factors  which  may  lead  to  total  destruction  of  the 
affected  and  sympathetic  affections  of  the  other  eye. 

In  rare  cases  corneal  wounds,  instead  of  healing  by  sim- 
ple infiltration,  produce  an  excessive  proliferation  of  cells, 
and  finally  necrosis  of  the  lips  of  the  wound.  The  conditions 
are  then  the  same  as  in  keratomalacia. 


b.   Wounds  ivith  the  Retention  of  a  Foreign  Body. 

A  foreign  body,  if  retained  in  the  cornea  after  having 
wounded  it,  always  produces,  unless  it  be  minutely  small,  a 
more  or  less  circumscribed  purulent  keratitis,  and  is  cast 
off  with  the  pus. 

Very  small  particles  of  metal  only,  and  sometimes  lime- 
salts,  are  permanently  retained  in  the  cornea.  They  are, 
however,  mostly  brought  there  by  the  use  of  eye-washes 
after  the  infliction  of  injury,  and  do  not  cause  it. 

Besides  these  inorganic  foreign  bodies,  organic  ones  ate 
sometimes  thrust  into  the  cornea  when  the  wound  is  in- 
flicted (or  during  ulcerative  processes),  and  it  seems  that 
they  are  retained  without  producing  a  lasting  inflammatory 


CORNEA. 


37 


reaction.  Among  them  are  the  particles  of  pigment  and  pig- 
mented cells,  as  above  mentioned,  parts  of  Descemefs  mem- 
brane, or  the  capsule  of  the  crystalline  lens  and  ciliae.  The 
latter  are  always  embedded  in  scar-tissue.  The  ciliae  are 
generally  found  to  be  surrounded  by  a  layer  of  epitheloid  or 
typical  epithelial  cells.     (See  Fig.  17.) 


Fio.  17.— Eye-lash  embedded  in  scar-tissue  witliin  the  cornea,  and  surrounded  by  epitheli- 
oid cells.    C.  Eye-lash. 

c.  Burns  with  Lime. 

Among  the  injuries  inflicted  upon  the  cornea,  burns  with 
lime  are  not  very  rare.  Gouvia  made  a  number  of  experi- 
ments to  study  their  exact  conditions.  According  to  his 
statements,  the  epithelial  cells  and  the  adjoining  lamellae  of 
the  cornea  become  perfectly  infiltrated  with  lime,  and  thus 
become  necrotic.  They  are  then  thrown  off  by  a  circum- 
scribed purulent  keratitis,  and  the  healing  process  is  the  same 
as  after  this  affection. 

Such  burns  of  the  cornea  are  very  frequently  combined 
with  similar  injuries  to  some  part  of  the  conjunctiva,  especially 
that  of  the  lids.  Since  the  conjunctival  ulcer  in  such  cases 
generally  lies  just  opposite  to  the  corneal  ulcer,  the  two 
surfaces  frequently  heal  together.     This  condition  is  called 


38 


THE  HUMAN  EYE. 


symblepharon,  if  only  a  part  of  the  conjunctiva  and  cornea 
are  united.  Extensive  burns  may  cause  the  whole  of  the 
conjunctival  surface  of  the  eye-lids  to  become  united  with 
the  eye-ball,  which  condition  has  received  the  name  of  an- 
chyloblepharon. 

C.  Regresssive  Metamorphoses. 

The  regressive  metamorphoses  which  are  observed  in  the 
cornea  (besides  those  found  in  scar-formations)  are  xerosis 
cornese  and  arcus  senilis. 

Xerosis  corneae  is  the  result  of  insufficient  moistening  of 
the  corneal  epithelium,  and  is  caused  by  conjunctival  diseases 
or  a  protrusion  of  the  eye-ball  of  such  a  degree  that  the  lids 
cannot  cover  it.  The  epithelium  becomes  irregular  in  appear- 
ance and  grayish,  and  under  the  microscope  is  found  to  be 
horny  and  dying.  This  metamorphosis  may  even  reach  the 
basal  layer  of  the  epithelium. 

Arcus  senilis  corneae,  the  marginal  dimness  of  the  cornea 
which  is  found  chiefly  in  old  people,  is  caused  by  fatty  de- 
generation of  the  lamellae  and  fixed  corneal  cells,  as  His  and 
Canton  have  described. 

D.   Tumors  of  the  Cornea. 

Although  a  large  number  of  so-called  tumors  have  been 
described  in  literature,  I  know  of  no  real  corneal  tumors,  and 
am  forced  to  doubt  the  corneal  origin  of  these  tumors,  the 
more,  since  hardly  any  of  them  involved  the  corneal  tissue 
alone.  So-called  corneal  tumors  generally  originate  in  the 
episcleral  tissue,  and  will  be  described  more  at  length  under 
that  head. 

Among  these  tumors  have  been  mentioned  :  papillomata, 
dermoid,  sarcomatous  and  cancroid  tumors,  fibromata,  and 
lately  a  granuloma  of  the  cornea  has  been  drawn  by  Pagen- 
stecher  and  Genth,  which  I  think  must  be  considered  as  a 
granuloma  of  the  iris. 


II. 

SCLEROTIC. 
I.    Normal  Condi noNS. 

The  tissue  of  the  sclerotic  is  fibrillar,  like  that  of  the  cor- 
nea. The  fibrillae,  however,  are  not  so  transparent.  They  are 
united  into  fascicles,  which  interlace  with  each  other  without 
the  regularity  and  parallelism  so  characteristic  of  the  cornea. 
Here  and  there  also  elastic  fibrillae  may  be  found  enclosed 
in  the  fascicles.  There  are  some  more  regularly  arranged 
fascicles  in  the  anterior  part  of  the  sclerotic  near  ScJilemms 
canal,  and  around  the  optic  papilla,  which  run  in  an  equa- 
torial direction  (circular  fascicles). 

The  same  cementing  substance,  we  met  with  in  the  cornea, 
unites  the  fibrillae  of  the  sclerotic  with  each  other  into  fas- 
cicles, and  these  again  with  each  other  into  layers. 

Furthermore,  we  find  similar  lymphatic  canals  embedded 
in  the  cementing  substance  of  the  sclerotic  as  we  do  in  the 
cornea.  In  consequence  of  the  irregular  arrangement  of  the 
sclerotic  fascicles  it  is,  however,  difficult  to  get  as  nice  a  view 
of  these  canals  as  in  the  cornea.  It  is,  however,  possible  and 
my  own  researches  support  Waldeyer  s  statements  on  this 
point,  that  parts  of  these  canals  can  be  seen  by  staining  the 
sclerotic  carefully  with  nitrate  of  silver.  The  best  specimens 
are  obtained  from  the  parts  of  the  sclerotic  adjoining  the 
cornea.  The  sclerotic  canals  have,  moreover,  also  lacunae, 
containing  fixed  cells.  The  latter  are  identical  with  those  of 
the  cornea  in  shape  and  situation.  They  are  flat  oval  bodies, 
with  an  oval  nucleus,  and  have  generally  small  offsets.  By  far 
the  most  of  these  sclerotic  cells  are  unpigmented.  There  are, 
however,  some  pigmented  ones  to  be  found  in  every  sclerotic 
around  the  entrance  of  the  optic  nerve.  In  the  eyes  of  the 
white  races  they  are  but  rarely  found  in  the  anterior  portion 
of  the  sclerotic  near  the  corneo-scleral  margin,  while  they  are 
never  wanting  in  the  eyes  of  the  negroes. 


40 


THE  HUMAN  E  YE. 


Besides  the  unpigmented  and  pigmented  fixed  cells,  the 
sclerotic  also  contains  a  comparatively  small  number  of 
wandering  (lymphatic)  cells,  which  are  in  no  way  different 
from  those  found  in  other  tissues. 

The  tendons  of  the  external  ocular  muscles,  and  the  ex- 
ternal sheaths  of  the  optic  nerve  insert  themselves  into  the 
sclerotic.  The  former  reach  this  membrane  at  very  acute 
angles,  and  may  be  seen  entering  in  the  shape  of  a  wedge, 
Loewig  states  that  the  tendons  of  the  recti  muscles,  after 
having  entered  the  sclerotic,  form  meridional  (longitudinal) 
fibres,  while  the  oblique  muscles  are  said  by  the  same  author 
to  form  equatorial  (circular)  fibres. 

The  sheaths  of  the  optic  nerve,  after  coalescing  with  the 
sclerotic,  form  part  of  the  equatorial  fibres  which  are  found 
nearly  regularly  around  the  entrance  of  the  optic  nerve  in 
this  membrane.  The  lymphatic  space,  which  is  enclosed 
between  the  sheaths  of  the  optic  nerve  (intervaginal  space), 
is  sometimes,  especially  in  myopic  eyes  {Von  Jaeger),  found 
to  enter  the  sclerotic,  severing  it  thus  somewhat  into  two 
layers. 

Earlier  authors  unanimously  described  a  large  round  hole 
in  the  sclerotic,  through  which  the  optic  nerve  was  said  to 
enter  the  eye-ball.  Such  a  hole,  however,  does  not  exist. 
The  bundles  of  nerve  fibres  which  constitute  the  optic  nerve, 
do  not  pierce  the  sclerotic  in  toto,  but  more  or  less  separately, 
so  that,  if  the  nerve-fibres  could  all  be  removed,  the  sclerotic 
in  this  place  would  have  the  appearance  of  a  sieve,  which  has 
given  to  it  the  name  of  lamina  cribrosa. 

The  inner  surface  of  the  sclerotic  is  covered  with  a  layer 
of  thin  flat  endothelial  cells,  which  are  quadrangular  or  poly- 
gonal. They  may  be  easily  brought  to  view  by  staining  with 
nitrate  of  silver.  This  endothelial  layer  is,  however,  not  per- 
fectly continuous,  since  it  is  pierced  by  a  considerable  number 
of  fibres,  which  unite  the  sclerotic  with  the  choroid.  Endo- 
thelial cells  are  also  found  lying  upon  these  fibres. 

The  exterior  surface  of  the  sclerotic  is  covered  with  the 
loose  episcleral  tissue,  the  fibres  of  which  enter  and  spring 
from  the  sclerotic.  Where  this  tissue  surrounds  Tennons 
space  it  is  covered  with  a  very  thin  layer  of  endothelial  cells. 


SCLEROTIC. 


41 


Anteriorly  this  episcleral  tissue  passes  over  into  the  conjunc- 
tiva bulbi. 

At  the  corneo-scleral  margin  the  fibres  and  lymphatic 
canals  of  the  cornea  go  over  into  the  fibres  and  canals  of  the 
sclerotic.  In  transverse  sections  of  this  part  of  the  eye-ball 
we  always  find  a  number  of  vessels.  Leber  described  them  as 
a  venous  plexus.  Although  I  do  not  doubt  the  existence  of 
such  a  venous  plexus,  I  must  agree,  on  the  other  hand,  with 
Schwalbe  and  Waldeyer,  who  maintain  the  existence  of  the  so- 
called  Schlemms  canal,  besides  the  venous  plexus  of  Leber. 
The  latter  is  generally  the  largest  of  the  vessels,  and  lies 
nearest  the  inner  surface  of  the  sclerotic.  It  is  lined  with  a 
layer  of  endothelial  cells,  and  the  corneo-scleral  fibres  which 
form  its  inner  wall,  are  fenestrated  in  the  manner  above  re- 
ferred to.  The  anterior  chamber  and  its  endothelium  are 
therefore  in  more  or  less  direct  communication  with  ScJileniins 
canal  and  its  endothelial  lining.  While  it  is  easy  to  fill  the 
venous  plexus  by  injecting  the  blood-vessels  with  a  colored 
fluid,  I  was  never  able  to  inject  ScJilemni  s  canal  from  this 
side.  It  is,  however,  comparatively  easy  to  fill  it  by  injecting 
a  tinted  fluid  into  the  anterior  chamber.  I  must  further  state, 
with  Waldeyer,  that  I  never  yet  found  blood,  which  is  hardly 
ever  wanting  in  the  vessels  of  the  venous  plexus,  in  this 
vessel : 

The  blood-vessels  of  the  sclerotic  proper  come  from  the 
anterior  and  posterior  ciliary  arteries.  Waldeyer  states  that 
they  are  all  surrounded  by  a  sheath,  called  by  him,  "  perithe- 
lium-sheath." 

The  nerves  of  the  sclerotic,  according  to  Helfreich,  are 
arranged  in  a  similar  manner  to  those  of  the  cornea.  His 
statement  has  not  yet  been  confirmed  by  others.  My  own 
researches,  by  staining  the  sclerotic  with  chloride  of  gold  and 
osmic  acid,  have  not  been  successful. 

The  vorticous  veins  (4,  5  or  6)  perforate  the  tissue  of  the 
sclerotic  at  an  acute  angle,  from  before  backwards.  They  are 
surrounded  by  a  lymphatic  sheath,  as  are  the  ciliary  arteries 
and  nerves,  passing  through  the  sclerotic,  which  opens  into 
the  suprachoroidal  space  on  one  side  and  Tennons  space  on 
the  other  side.     The  cilary  nerves,   while  passing  through 


42  THE  HUMAN  E  YE. 

their  canals  in  the  sclerotic,  are  frequently  accompanied  by 
posterior  ciliary  arteries,  which  is  of  great  importance  in  the 
pathological  processes  observed  in  these  organs. 

2.  Pathological  Conditions 

A.  Scleritis  and  its  Results. 

Scleritis,  like  keratitis,  is  histologically  characterized  by  a 
larger  number  of  round-cells,  which  may  leave  the  fibres  of 
the  sclerotic  intact,  and  only  separate  them  slightly  from  each 
other,  or  may  entirely  destroy  them.  True,  scleritis  is,  it 
seems,  never  a  primary  disease,  unless  caused  by  an  injury; 
it  seems  to  be  always  caused  by  an  inflammatory  process  in 
the  neighboring  tissues.  There  are  two  kinds  of  scleritis, 
viz.,  infiltration-scleritis,  and  purulent-scleritis.  The  large 
number  of  blood-vessels  piercing  the  sclerotic  are  in  such  cases 
of  inflammation  hyperaemic,  and  sometimes  new  blood-vessels 
are  seen  to  spring  from  them.  Infiltration-scleritis  is  always 
of  a  chronic  character,  and  by  aggravation  may  become  puru- 
lent. 

a.  hifiltratioti-Scleritis. 

Infiltration-scleritis  is  always  found  in  the  parts  of  the 
sclerotic  which  are  pierced  by  blood-vessels.  It  affects  the 
fibres  of  the  sclerotic  comparatively  little,  if  at  all.  The 
primary  diseases  leading  to  it  are  corneal  affections,  iritis, 
iridocyclitis,  not  purulent  choroiditis,  and  intra-ocular  new- 
formations.  From  this  it  is  evident,  that  we  shall  find  infil- 
tration-scleritis chiefly,  or  perhaps  only,  at  the  corneo-scleral 
margin,  and  where  the  vasa  vorticosa,  the  posterior  and 
anterior  and  ciliary  arteries  perforate  the  sclerotic.  We  then 
find  these  blood-vessels  in  a  state  of  hyperaemia,  and  fre- 
quently, in  higher  degrees  of  inflammation,  always  new-formed 
vessels  starting  from  them  and  entering  the  tissue  of  the 
sclerotic.  The  interstices  between  the  fibres  of  this  latter 
membrane  are  filled  with  round-cells.  I  am,  however,  not 
able  to  state  whether  these  cells  (like  those  found  in  the  cornea 
during  keratitis)  are  immigrated  as  well  as  proliferated  ones 


SCLEROTIC.  43 

from  the  fixed  scleral  cells.  It  is  certainly  very  probable  that 
they  also  come  from  both  sources.  Infiltration-scleritis  gen- 
erally involves  the  whole  thickness  of  the  sclerotic,  and  may 
reach  into  the  episcleral  tissue. 

When  the  primary  disease  heals,  the  scleritis  generally 
also  disappears,  without  leaving  a  trace.  In  other  cases,  how- 
ever, if  the  primary  disease  is  of  a  very  chronic  kind,  the 
sclerotic  begins  to  become  stretched  and  atrophic  (staphy- 
loma), or  a  new-formation  of  connective-tissue  takes  place 
between  its  fibres,  which  leads  to  an  hypertrophic  condition, 
such  as  we  find,  for  instance,  in  the  sclerotic  of  phthisical  eye- 
balls. Wounds  of  the  sclerotic  also  heal  with  the  symptoms 
of  infiltration-scleritis.     (See  later  on.) 

b.  Piirulcnt  Scleritis. 

The  characteristic  feature  of  purulent  scleritis,  is  an  abund- 
ance of  round-cells,  which  causes  a  rapid  destruction  of  the 
fibres  of  the  sclerotic.  This  kind  of  scleritis  also  attacks  by 
preference  the  placet  where  the  sclerotic  is  pierced  by  blood- 
vessels and  nerves.  Purulent  scleritis  generally  originates 
from  purulent  affections  of  the  uveal  tract,  and  is  one  of  the 
symptoms  of  purulent  panophthalmitis.  It  may  also  be 
caused  by  foreign  bodies.  I  have  never  had  occasion  to  see 
a  genuine  abscess  such  as  we  find  in  the  cornea  in  the  scler- 
otic. Purulent  panophthalmitis  is  sometimes  incorrectly 
called  scleral  abscess. 

Since  purulent  scleritis  is,  as  a  rule,  caused  by  purulent 
affections  of  the  uveal  tract,  it  is  not  astonishing  that  it 
chiefly  (and  often  only)  involves  the  inner  layer  of  the  scler- 
otic. In  consequence  of  circumscribed  abscess-like  cell-aggre- 
gations in  the  choroid,  which  mostly  perforate  the  lamina 
vitrea  and  enter  the  vitreous  body,  a  very  small  part  of  the 
sclerotic  may  become  ulcerated.  In  such  a  place  the  puru- 
lent inflammation  may  then  cause  an  excessive  new-formation 
of  connective-tissue,  which  may  grow  through  the  choroid 
and  retina  into  the  vitreous  body. 

The  inflammation,  however,  does  not  always  remain  con- 
fined only  to  such  a  circumscribed  part,  or  to  the  inner  layers 
of  the  sclerotic,  but  the  new-formation  of  cells,  and  with  it 


44 


THE  HUMAN  E  YE. 


necrosis  of  the  sclerotic  tissue,  may  progress,  until  this  mem- 
brane becomes  perforated  on  its  outer  surface.  Such  perfora- 
tions usually  happen  in  the  region  of  the  equator  of  the 
globe,  where  the  vasa  vorticosa  pierce  the  sclerotic. 

Although  this  kind  of  inflammation  of  the  sclerotic  is 
generally  chronic,  it  is  in  rare  cases  found  to  run  its 
course  in  a  very  acute  manner.  In  these  cases  the  new- 
formation  of  cells  is  so  excessive,  that  the  destruction  of  the 
fibres  of  the  sclerotic  cannot  go  hand  in  hand  with  it.  Con- 
sequently this  membrane  must  become  very  much  thick- 
ened, and  may,  therefore,  be  mistaken  for  total  staphyloma 
of  the  sclerotic. 

I  had  the  opportunity  to  examine  such  an  eye,  which  was 
enucleated  in  a  homoeopathic  eye-hospital  with  the  diagnosis 
of  total  staphyloma  of  the  sclerotic,  and  was  shown  to  me  as 
a  highly  interesting  and  rare  case  of  acute  staphyloma  with 
hypertrophy  of  the  sclerotic.  It  is  true,  to  the  naked  eye 
the  sclerotic  appeared  to  be  about  six  times  as  thick  as  a 
normal  one.  The  microscope,  however,  revealed  at  once  an 
immense  number  of  round-cells  which  lay  between  the  fibres 
of  the  sclerotic  in  the  episcleral  tissue,  and  pressed  these 
fibres,  which  were  not  as  yet  necrotic,  far  apart. 

In  case  the  sclerotic  becomes  perforated  in  a  circumscribed 
spot,  the  pus  escapes  on  its  outer  surface,  and  choroid  and 
retina  become  adherent  to  the  scar-tissue,  which  afterwards 
closes  the  perforation.  The  result  of  such  a  perforation,  with 
subsequent  synechia  between  sclerotic,  choroid  and  retina, 
may  be  staphyloma. 

As  was  above  stated,  purulent  scleritis  is  chiefly  found 
in  the  parts  surrounding  the  blood-vessels  and  nerves  which 
pass  through  it ;  and  this  inflammation  may,  too,  become 
the  cause  of  sympathetic  affections  in  the  fellow-eye. 

The  Results  of  Scleritis. 
a.  Formation  cf  Scars. 

Scars  in  the  sclerotic  are  only  found  in  consequence  of 
purulent  scleritis.    The  conditions  are  then  the  same  as  when 


SCLERO  TIC. 


45 


the  sclerotic  has  been  pierced  by  an  injury,  and  will  be  treated 
of  under  that  head. 

b.  Prolapse  and  Incarceration  of  Iris,  Ciliary  Body,  Choroid, 
Retina,  Crystalline  Lens  and  Vitreous  Body  in  the  Sclerotic. 

These  conditions  will  also  be  spoken  of  in  the  chapter  on 
injuries  of  the  sclerotic. 

c.  Hypertrophy  of  the  Sclerotic. 

A  chronic  inflammatory  process  of  the  whole  eye-ball, 
or  of  the  uveal  tract,  frequently  causes  chronic  infiltra- 
tion-scleritis  leading  to  new-formation  of  connective-tissue, 
which  produces  a  hypertrophic  condition  of  the  sclerotic. 
From  the  fact  that  it  is  impossible  at  a  later  period  of  these 
affections  to  find  cellular  elements  in  the  hypertrophied  con- 
nective-tissue, and  since,  moreover,  the  lymphatic  canals  and 
their  lacunae  are  then  more  or  less  obliterated,  we  may  with 
some  probability  conclude  that  the  fixed  cells  of  the  sclerotic 
take  an  active  part  in  the  new-formation  of  this  connective- 
tissue.  It  is  not  impossible,  however,  that  they  are  destroyed 
only  during  the  period  of  retraction  of  the  new-formed  tissue. 
In  spite  of  this  retraction,  the  sclerotic  sometimes  remains 
considerably  thickened.  This  hypertrophic  condition  of  the 
sclerotic  always  precedes  total  phthisis  of  an  eye-ball,  and 
the  process  leading  to  it  begins,  without  exception,  in  the 
posterior  parts  of  the  sclerotic,  around  the  entrance  of  the 
optic  nerve. 

The  blood  and  lymphatic  vessels  become  obliterated,  and 
this  again  results  in  grave  disturbances  in  the  nutrition  of 
the  interior  of  the  eye-ball.  Later  on,  the  hypertrophy  pro- 
gresses more  and  more  towards  the  corneo-scleral  margin,  and 
in  the  highest  degrees  of  phthisis  of  the  globe  nearly  the 
whole  of  the  sclerotic  is  equally  thickened.  It  frequently 
happens  that  while  this  is  going  on,  inflammatory  processes 
in  the  interior  of  the  globe,  which  produce  shrinking,  force 
the  sclerotic  to  fold  itself.  The  episcleral  tissue  in  such  cases 
is  also  nearly  always  inflamed,  and  takes  an  active  part  in 
the  new-formation  of  connective-tissue,  and  sometimes  Ten- 
nons  space  thus  becomes  perfectly  obliterated. 


46 


THE  HUMAN  EYE. 


In  examining  two  eyes  which  were  enucleated  in  conse- 
quence of  gun-shot  wounds,  and  were  in  the  earher  stages  of 
phthisis,  I  had  an  opportunity  to  find  alterations  in  the  pos- 
terior ciliary  blood-vessels  within  the  sclerotic,  which  show 
that  these  blood-vessels  not  only  become  obliterated  by 
pressure  exerted  upon  them  by  the  shrinking  new-formed 
connective-tissue,  but  that  they  may,  moreover,  take  an  active 
part  in  this  new-formation.  I  found  the  endothelium  of  these 
vessels  in  a  high  degree  of  proliferation.  Its  cells  were  en- 
larged and  had  several  nuclei,  and  they  filled  the  whole  of  the 
lumen  of  each  vessel  so  altered.  In  some  of  them  I  also 
found  giant-cells  with  from  six  to  fifteen  nuclei.     While  most 


Fig.  i8. — Blood-vessels  of  the  sclerotic  from  a  wounded  eye  in  the  process  of  phthisis  bulbi. 
A.  Proliferation  of  the  endothelial  cells,  i.  Giant-cells.  B.  Transformation  into  con- 
nective-tissue. 

of  the  changed  endothelial  cells  appeared  round  and  vesicle- 
like, some  of  them  had  one  or  two  offsets,  and  passed  gradu- 
ally over  into  the  spindle  shape.     (See  Fig.  i8.) 

d.  Atrophy  of  the  Sclerotic  and  Ectasy  {Staphyloma  of  the 

Sclerotic). 

Both  kinds  of  scleritis  (but  especially   infiltration  scler- 
itis)  very  frequently   produce  staphyloma  of  the  sclerotic. 


SCLERO  TIC. 


47 


The  characteristic  features  of  this  affection  are  atrophy  and 
stretching  of  the  scleral  tissue.  Although  synechias  between 
the  sclerotic  and  some  part  of  the  uveal  tract  are  very  fre- 
quent in  cases  of  such  staphyloma,  they  are  not  always 
found,  and  are  therefore  not  essential.  This  atrophy  and 
ectasy  may  concern  only  a  part  of  the  sclerotic  or  the  whole 
of  it.  We  have  therefore  a  total  and  a  partial  staphyloma 
sclerae. 

Total  staphyloma  of  the  sclerotic  is  but  seldom  observed, 
and  then  it  forms  only  a  part  of  the  total  ectasy  of  the  eye- 
ball. We  find,  in  these  eyes,  an  abnormal  extenuation  and 
stretching  of  the  sclerotic,  which  may  occasionally  be  com- 
bined with  adhesions  between  this  membrane  and  the  uveal 
tract.  Even  where  such  adhesions  are  wanting,  the  uveal 
tract  shows  varying  pathological  alterations.  All  the  blood- 
vessels which  either  nourish  the  sclerotic  or  only  pass  through 
it  become,  as  a  rule,  obliterated.  Also  the  nerves  gradually 
disappear,  but  generally  much  later  than  the  blood-vessels. 

Partial  scleral  staphyloma  is  of  frequent  occurrence,  and 
a  characteristic  feature  of  it  is,  that  we  nearly  always  find 
an  adhesion  between  the  uveal  tract  and  the  bulging  part  of 
the  sclerotic.  It  may,  of  course,  be  found  in  any  part  of  the 
sclerotic.  The  following  are  the  three  kinds  most  frequently 
observed. 

I.  Anterior  Staphylo7na  of  the  Sclerotic. 

Concerns  those  parts  of  the  sclerotic  which  lie  in  front 
of  the  equator  of  the  eye-ball.  There  are  two  varieties, 
viz.^  corneo-scleral  and  ciliary  staphyloma. 

a.  Corneo-Scleral  Staphyloma  {^formerly  called  Intercalar- 
Staphylojna). 

This  form  of  staphyloma  lies  in  the  beginning  just  at  the 
corneo-scleral  margin.  In  all  such  cases  which  I  have  ex- 
amined, I  found  iritis  or  iridocyclitis  either  to  be  present,  or 
unmistakable  signs  that  they  had  existed.  The  periphecal 
parts  of  the  iris  are  united  to  the  corneo-scleral  tissue  by  a 
fine  layer  of  newly-formed  connective-tissue,  which  is  formed 


48 


THE  HUMAN  EYE. 


by  the  proliferating  endothelial  cells  of  Desceniei's  membrane 
and  the  anterior  surface  of  the  iris.  In  consequence  of  this 
adhesion  of  the  anterior  surface  of  the  peripherical  part  of 
the  iris  with  the  corneo-scleral  tissue,  Fontanas  spaces  become 
obliterated.  During  the  progress  of  the  new-formation  the 
ligamentum  pectinatum  and  the  periphery  of  Descemefs 
membrane  are  obliterated,  and  since  the  soft  tissue  of  the 
iris  cannot  replace  the  resistance  which  is  lost  with  the  dis- 
appearance of  Descemefs  membrane,  these  parts  become 
gradually  stretched  and  atrophied.  Their  blood-vessels  and 
lymphatic  canals  are  found  obliterated. 

The  stretching  of  these  parts  (where  the  iris  is  adherent 
to  the  corneo-scleral  tissue  gradually,  removes  the  free  part 
of  the  iris  from  the  ciliary  body.  If  the  affection  progresses 
still  farther,  more  and  more  of  the  anterior  surface  of  the  iris 
becomes  adherent  to  Descemefs  membrane  and  more  and 
more  of  the  latter  membrane  is  destroyed.  This  leads,  of 
course,  to  a  gradual  diminution  of  the  area  of  the  free  iris, 
and  the  size  of  the  anterior  chamber,  and  furthermore  to 
dilation  of  the  pupil,  which  is  alway  sobserved  in  such  eyes. 
(See  Fig.  19.) 


Fig.  19. — Corneo-scleral  staphyloma,  i.  New  insertion  of  the  iris  which  adheres  to  Des- 
cemefs membrane  by  means  of  a  tissue  formed  from  the  endothelial  cells.  2.  The 
ectatic  part ;  the  membrana  Descemetii  has  disappeared. 


b.  Ciliary  Staphyloma. 

Ciliary  staphyloma  concerns  the  ciliary  region  only,  and 
involves  the  ciliary  body  and  the  part  of  the  sclerotic  cover- 
ing it.     The  affection  takes  its  origin  from  a  chronic  cyclo- 


SCLERO  TIC. 


49 


sderitis.  This  leads  to  an  adhesion  between  the  ciliary  body 
and  the  sclerotic,  and  to  atrophy  and  stretching  of  these  parts. 
The  muscular  tissue  of  the  ciliary  body  disappears  totally  in 
the  later  stages  of  this  process,  and  we  frequently  find  only  a 
layer  of  pigmented  cells  lining  the  bulging  parts,  as  the  re- 
mains of  this  body.  The  staphyloma  is  often  bounded  ante- 
riorly by  some  atrophic  ciliary  processes,  while  posteriorly  it 
slopes  gradually  down  into  the  more  or  less  normal  equato- 
rial region.  The  blood-vessels  and  lymphatic  canals  of  the 
involved  parts  are,  of  course,  again  found  to  be  obliterated 
and  the  nerves  atrophied.     (See  Fig.  20 ) 


Fig.  2o.— Ciliary  staphyloma.    Ciliary  body  adherent  to  the  sclerotic  and  atrophic.    Be- 
ginning ectasia. 

Both  of  these  two  kinds  of  anterior  staphyloma  of  the 
sclerotic  are  frequently  seen  to  travel  around  the  whole  of 
the  circumference  of  the  eye-ball,  and  have  therefore  been 
called  *'  annular  "  staphylomata. 

2.  Equatorial  Staphyloma  of  the  Sclerotic. 

This  form  of  scleral  staphyloma  lies  either  just  in  the 
equator  of  the  globe  or  a  little  behind  it.  It  is  caused  by 
chronic  chorio-scleritis  leading  to  adhesion  between  choroid 
and  sclerotic  and  atrophy,  and  is  mostly  found  just  where,  in 
the  normal  eye,  a  vorticous  vein  passes  through  the  sclerotic. 
The  histological  conditions  are  the  same  as  in  the  other  forms 
of  scleral  staphyloma. 

3.  Posterior  Staphyloma  of  t]ie  Sclerotic. 

Is  the  result  of  a  chronic  sclerochorioiditis,  which, 
however,  does  not  always  leads  to  an  adhesion,  and  which 
is  nearly  without  exception  confined  to  region  of  the  optic 


50 


THE  HUMAN  E  YE. 


nerve  and  macula  lutea.  Sometimes  it  is  caused  by  a  con- 
genital defect.  Since  the  point  of  direct  vision  (the 
macula  lutea)  is  gradually  more  and  more  removed  from  the 
anterior  surface  of  the  globe  in  consequence  of  the  staphy- 
loma, it  influences  vision  in  a  very  important  way,  viz.,  it 
makes  the  eye  myopic.  The  histological  conditions  are  also 
here  in  no  way  different  from  what  has  been  described  above. 
(See  Fig.  21.) 


Fig.  21.— Posterior  staphyloma  from  a  myopic  eye.    Ciioroid  and  sclerotic  adhere  to  each 
other  and  are  atrophic. 

All  these  different  varieties  of  staphyloma  of  the  sclerotic 
may  at  any  time  become  stationary.  In  rare  cases  they  pro- 
gress, until  the  eye  becomes  ruptured.  In  this  way,  and 
in  consequence  of  changes  in  the  interior  of  the  eye-ball, 
such  staphylomata  lead  to  total  destruction  of  the  organ. 
Staphylomata  also  usually  cause  an  increase  of  the  intra- 
ocular pressure  (glaucoma),  with  all  its  consequences.  This 
is  probably  due  to  the  alterations  in  the  uveal  tract,  and 
especially  to  the  obliteration  of  so  many  lymphatic  canals 
and  blood-vessels,  by  which  the  veinous  blood  and  lymphatic 
fluids  ought  to  be  carried  out  of  the  eye.  Glaucoma  is  chief- 
ly caused  by  anterior  and  equatorial  scleral  staphylomata. 
Since  in  posterior  staphyloma  the  choroid  is  less  frequently 
found  to  adhere  to  the  sclerotic,  and  it  is  generally  confined 
to  a  smaller  part  of  the  eye ;  and,  moreover,  seems  rather 
to  influence  the  entrance  than  the  exit  of  the  blood  from 
the  eye-ball,  glaucoma  is  but  seldom  found  these  eyes. 
This  latter  argument  seems  especially  to  be  proven  by 
the  experiments  of  Kniess,  which  led  this  author  to  the 
conclusion,    that    the    lymphatic    fluids  in   the    eye-ball    run 


SCLEROTIC.  t\ 

from  behind  forward.  I  cannot,  however,  agree  with  the 
views  of  the  same  author  when  he  finds  the  universal 
cause  of  glaucoma  in  the  obliteration  of  Fontanas  spaces 
As  I  have  stated,  glaucoma  is  frequently  found  as  a  conse- 
quence of  all  these  different  kinds  of  staphyloma,  especially 
anterior  scleral  staphylomata,  I  have,  however,  examined 
quite  a  number  of  glaucomatous  eyes  which  showed  no  oblit- 
eration of  Fontanas  spaces,  that  is,  no  corneo-scleral  staphy- 
loma. 

The  great  influence  exerted  by  all  forms  of  scleral 
staphyloma  upon  the  nerves  of  the  affected  eye  makes  it 
evident  that  they  are  frequently  the  cause  of  sympathetic 
affections  of  the  fellow-eye. 

Several  authors  have  observed  deposits  of  lime  in  the 
sclerotic,  and  even  osseous  formations,  in  consequence  of 
chronic  scleritis  have  been  described.  Coccins  and  others 
found  a  fatty  degeneration  of  the  sclerotic  analogous  to  the 
arcus  senilis  of  the  cornea.  I  never  have  seen  any  one  of 
these  affections. 

B.  Injuries  to  the  Sclerotic  and  their  Results. 

a.  Wounds  ivitJiout  Subsequent  Retention  of  a  Foreig7i  Body. 

We  have  to  speak  under  this  head  of  ruptures  of  scler- 
otic and  wounds  caused  by  cutting  instruments. 

The  healing  process  after  the  infliction  of  such  injuries  to 
the  sclerotic  greatly  resembles  those  observed  in  the  cornea 
under  similar  circumstances.  Very  soon  after  the  injury  has 
been  received  the  blood-vessels  become  hypersemic,  and  the 
edges  of  the  lips  are  infiltrated  with  round-cells.  We  then 
find  the  same  histological  conditions  as  in  genuine  infiltration- 
scleritis.  Somewhat  later  a  fibrinous  exudation  into  the  canal 
of  the  wound  takes  place,  and  this,  too,  becomes  filled  with 
round-cells,  and  is  gradually  transformed  into  connective-tissue. 
The  new-formed  tissue  then  becomes  denser  and  begins  to 
shrink.  This  scar-tissue  nearly  always  runs  in  a  direction  which 
is  different  from  the  general  one  of  the  fibres  of  the  sclerotic, 
and  therefore  always  admits  of  an  easy  diagnosis  with  the  mi- 
croscope.    (See  Fig.  22.)     The  result  is  the  same  whether 


52 


THE  HUMAN  E  YE. 


Fig.  2J — Scar  in  the  sclerotic. 


the  instrument  pierces  the  whole  thickness  of  the  sclerotic 
or  only  a  part  of  it,  or  when  purulent  processes  have  pro- 
duced perforation  or  partial  ulceration   of  this  membrane. 

As  purulent  processes, 
which  lead  to  perforation 
of  the  sclerotic,  are,  as  a 
rule,  finished  as  such  as 
soon  as  the  perforation 
has  taken  place,  we  then, 
usually  find,  only  the 
symptoms  of  infiltration- 
scleritis.  The  healing  process  is  in  such  cases  as  described 
above. 

Since,  however,  an  injury  or  rupture  of  the  sclerotic  but 
seldom  occurs,  which  does  not  also  at  the  same  time  affect 
at  least  one  of  the  neighboring  membranes,  the  healing-pro- 
cess may  be  a  more  complicated  one,  and,  in  fact,  is  so  in  most 
cases.  If  the  injury  has  been  inflicted  from  the  outside,  at 
least  the  conjunctiva  bulbi  must  also  be  wounded  ;  but  the 
injury  may  just  as  well  pierce  all  the  internal  membranes  of 
the  globe  and  the  vitreous  body.  If  the  wound  of  the  scle- 
rotic is  received  from  its  inner  surface,  the  inflicting  instru- 
ment must  have  passed  through  nearly  all  the  remaining 
parts  of  the  eye  before  reaching  it.  In  this  way  a  great 
many  variations  and  complications  may  be  observed  during 
the  healmg  process.  The  most  frequent  complication  is  the 
prolapse,  and  afterwards  incarceration  in  the  sclerotic  of  the 
iris,  the  ciliary  body  or  choroid.  The  histological  conditions 
in  these  cases  are  the  same  as  those  we  found  in  incarcera- 
tion of  the  iris  in  the  cornea.  In  rare  cases  one  of  these 
parts  of  the  uveal  tract  may  simply  become  adherent  to 
the  wound  in  the  sclerotic.  Furthermore,  we  may  find 
the  crystalline  lens,  the  retina  and  the  vitreous  body  pro- 
lapsing into  the  scleral  wound.  If  the  injury  did  not  at  the 
same  time  rupture  the  capsule  of  the  crystalline  lens,  the 
latter  may  escape  in  toto  through  the  wound,  and  remain 
lodged  under  the  conjunctiva.  If  the  capsule  has  been  rup- 
tured, the  same  may  take  place,  or  the  crystalline  lens,  after 
prolapsing  into  the  scleral  wound,  may  there  become  adher- 


SCLEROTIC. 


53 


ent.  During  the  healing  process  the  lens-substance  is  then, 
as  a  rule,  absorbed,  and  later  on  we  find  only  the  capsule 
embedded  in  the  scar.  If  prolapse  of  the  retina  has  oc- 
curred, this  membrane  always  takes  part  in  the  formation  of 
the  scar-tissue,  and  its  nervous  elements  disappear.  The 
vitreous  body,  also,  where  it  is  caught  in  the  wound,  is  trans- 
formed into  connective-tissue,  and  becomes  adherent  to  the 
scar. 

When  the  injuring  instrument  reaches  the  sclerotic  from 
its  inner  surface,  it  must,  as  stated,  have  pierced  the  vitreous 
body,  retina  and  choroid  before  reaching  the  sclerotic.  We 
therefore  find  in  such  cases  all  these  parts  adherent  to  the 
sclerotic,  whether  the  injury  concerns  the  whole  or  only  a 
part  of  the  thickness  of  this  membrane. 

Whenever  the  uveal  tract  has  also  been  injured,  or  has 
only  prolapsed  into  the  wound  of  the  sclerotic,  we  find  mole- 
cules of  pigment  in  the  lymphatic  canals  of  the  sclerotic  ad- 
joining the  wound.  Haemorrhages  of  varying  size  of  the 
wound-lips  are  of  frequent  occurrence,  and  are  absorbed 
during  the  healing  process. 

b.   Wounds  with  Subsequent  Retention  of  a  Foreign  Body. 

Since  the  scleral  tissue  is  a  great  deal  more  tolerant  of 
injuries  than  the  tissue  of  the  cornea,  we 
very  frequently  find  foreign  bodies  embed- 
ded in  the  sclerotic  without  causing  any 
serious  reaction.  Where  such  reaction 
takes  place,  a  circumscribed  purulent  scler- 
itis  ensues,  during  which  the  foreign  body 
is  thrown  off  with  the  pus. 

The  more  common  result  is,  that  in 
consequence  of  chronic  infiltration-scleritis 
new-formation  of  connective-tissue  takes 
place,  in  which  the  foreign  body  becomes 
embedded.  All  the  injured  membranes 
take  part  in  the  formation  of  this  tissue. 
(See  Fig.  23.) 

Scars  in  the  sclerotic  may  become  ec- 
tatic  and  lead  to  scleral  staphyloma.  f''^/  !^r'f?''^'P  ^°'^>'  1?"' 

^    J  emDedded  in  the  sclerotic. 


54 


THE  HUMAN  E  YE, 


Since  most  of  the  scleral  injuries  at  the  same  time  involve 
a  part  of  the  uveal  tract,  they  may  produce  sympathetic 
affections  of  the  fellow-eye. 

C.  Tumors  of  the  Sclerotic. 

Fibroma,  sarcoma  and  osteoma  of  the  sclerotic  have  been 
described.  They  were  all  found  at  the  corneo-scleral  margin, 
and  certainly  were  tumors  of  the  episcleral  tissue. 


III. 

CONJUNCTIVA   BULBI   AND    EPISCLERAL 

TLSSUE. 

I.  Normal  Conditions. 

The  epithelium  which  covers  the  conjunctiva  bulbi  is 
always  thicker  near  the  cornea-scleral  margin  than  it  is  farther 
backward.  The  peculiar  superficial  epithelial  layer  of  the  con- 
junctiva palpebrarum,  consisting  of  cylinder  and  cone-shaped 
cells,  is  more  and  more  changed  into  a  layer  of  flat  cells,  like 
the  superficial  layer  of  the  corneal  epithelium,  the  nearer  it 
comes  to  the  corneo-scleral  margin,  and  we  find  nearest  the 
cornea  several  layers  of  flat  cells  with  an  oval  nucleus,  which 
frequently  have  one  or  two  nucleoli.  The  more  cuboid  epi- 
thelial cells  of  the  inner  layer  of  the  conjunctiva  palpebrarum 
remain  very  much  the  same,  until  they  join  the  basal  layer 
of  the  corneal  epithelium.  Near  the  corneo-scleral  margin 
we  find  at  first  a  small,  then  rapidly  increasing  intermediate 
layer,  consisting  of  the  same  forms  of  cells  which  we  found  in 
the  middle  layer  of  the  corneal  epithelium.  Just  where  the 
conjunctiva  joins  the  cornea — that  is,  where  Botvmans  layer 
of  the  cornea  begins — the  epithelium  forms  two  or  three  pa- 
pillae, which  dip  into  the  underlying  tissue. 

The  so-called  mucous-cells  peculiar  to  the  epithelium 
of  the  conjunctiva  are  especially  numerous  upon  the  con- 
junctiva bulbi.  They  are  to  be  considered  as  metamor- 
phosed epithelial  cells  {Waldeyer),  and  are  large,  round, 
vesicle-like  bodies.  When  viewed  from  above  they  ap- 
pear as  round  circles,  and  seem  to  contain  a  transparent 
fluid.  In  transverse-sections  they  show  the  same  shape  as 
the  "  goblet-cells  "  of  the  intestinal  tract,  and  are  found  to 
have  their  base  in  the  basal  layer  of  the  epithelium. 

Among  the  cells  of  the  basal  layer,  nearer  the  cornea  and 
the  middle  layers,  I  found  frequently  cells  with  two  nuclei  or 
cells  which  show  evident  signs  of  being  of  a  recent  date.    It 


56  THE  HUMAN  EYE. 

appears  therefore  that  the  regeneration  of  the  epethelial  cells 
of  the  conjunctiva  takes  place  in  the  same  way  as  it  does  in 
the  cornea. 

Under  this  epithelium  lies  a  tissue  which  by  clinicists  is 
usually  considered  to  form  two  layers,  viz.,  the  subconjunc- 
tival and  the  episcleral  tissue.  Histologically  such  a  separa- 
tion does  not  exist.  There  is  only  one  conjunctival  or 
episcleral  tissue,  and  we  may  yield  to  the  clinicists  only  so 
far  as  to  call  the  part  of  this  tissue  which  lies  close  to  the 
sclerotic,  episcleral,  and  the  part  just  under  the  epithelium, 
subconjunctival.  Near  to,  and  just  at  the  corneo-scleral 
margin,  the  possibility  of  even  such  an  ideal  separation  is 
wanting. 

The  conjunctival  tissue  is  formed  by  a  network  of  fine 
connective-tissue  fibres  and  elastic  fibrillae. 

The  meshes  of  this  network  of  fibres  are  comparatively 
wide,  except  just  under  the  epithelium  and  upon  the  sclero- 
tic, where  they  become  smaller  and  the  tissue  denser.  This 
condensation  is  caused  by  additional  fibres  coming  from 
Bowman  s  layer  and  the  sclerotic,  which  enter  the  conjunc- 
tiva. I  observed  above,  that  the  fibres  of  the  conjunctival 
tissue  enter  the  sclerotic.  Within  the  meshes  of  the  con- 
junctiva lie  a  number  of  cells  of  two  distinct  kinds.  The 
first  are  flat  cells  and  nuclei,  which  are  adherent  to  the  fibres, 
probably  belong  to  the  class  of  endothelial  cells,  and  are 
comparatively  rare.  The  second  are  lymphatic  cells,  sus- 
pended in  the  fluid  which  fills  the  interstices,  and  generally 
lie  together  in  small  clusters.  These  cells  are  more  numer- 
ous in  the  conjunctiva  than  in  other  tissues,  and  give  it  the 
typical  structure  of  what  by  older  anatomists  was  called 
adenoid  tissue.  I  have  never  seen  lymphatic  follicles  in 
the  normal  human  zox\]\xr\zX\v^{Waldeyer). 

Small  clusters  of  fat-cells  have  also  been  found  by  Wal~ 
deyer  in  the  conjunctival  tissue. 

The  small  yellowish  tumor  which  is  so  frequently  seen  on 
the  inner  or  outer  side  of  the  cornea-scleral  margin,  in  that 
part  of  the  conjunctiva  bulbi  which  lies  just  behind  the  pal- 
pebral fissure,  has  wrongly  been  called  Pinguecula,  as  it  was 
thought  to  consist  of  fat-tissue.     Scemisch  changed  this  name 


CONJUNCTIVA  BULB!  AND  EPISCLERAL   TISSUE.        57 

into  "  palpebral  fissure-spot  "  (Lidspaltenfieck).  The  little 
tumor  consists  chiefly  of  very  dense  connective-tissue, 
which  contains  scarcely  any  blood-vessels  or  cells,  and  is 
covered  by  a  strangely  thick  layer  of  epithelial  cells.  I 
always  found  among  these  epithelial  cells  such  a  large  num- 
ber of  serrated  ones  that  the  condition  was  very  similar  to 
that  of  an  epithelial  tumor.  The  erroneous  opinion,  that 
this  tumor  consisted  of  fat-tissue,  was  first  corrected  by 
Weller  and  Robin. 

The  blood-vessels  of  the  conjunctiva  all  come  from  the 
anterior  ciliary  blood-vessels.  Their  structure  has  nothing 
peculiar.  They  are  very  numerous,  especially  in  the  sub- 
conjunctival tissue,  and  the  veins  have  a  comparatively  wide 
lumen.  The  capillary  blood-vessels  which  lie  under  the  epi- 
thelium form  an  irregular  network  with  small  interstices. 
Contrary  to  Wa/dej/er,  I  cannot  find  any  papillae  {Gefasspa- 
pillen)  in  the  conjunctiva  bulbi. 

The  nerves  of  the  conjunctiva  bulbi  first  form  a  net- 
work of  non-medullated  fibres  under  the  epithelium  {J.  Ar- 
7iold)  and  then  enter  the  latter.  Longworth  has  lately  been 
able  to  prove  beyond  doubt,  that  these  nerves  really  end 
in  peculiar  little  bulbous  structures  (Endkolben),  as  first  de- 
scribed by  Krause  and  denied  by  a  large  number  of  exam- 
iners, especially  J.  A  rno/d  and  Waldeyer. 

The  lymphatic  vessels  of  the  conjunctiva  are  {Waldeyer 
and  others)  in  direct  communication  with  the  corneal  and 
scleral  canals,  which  is  a  very  important  fact  in  pathological 
processes. 

2.  Pathological  Conditions. 

Before  speaking  of  the  different  kinds  of  inflammation  of 
the  conjunctiva,  I  would  like  here  to  mention  that  kind  of 
oedema  of  the  conjunctiva  which  is  clinically  known  as  in- 
filtration-oedema, and  is  found  so  frequently  after  operations 
and  wounds  near  the  cornea-scleral  margin,  especially  when 
the  conjunctival  wound  is  healed  and  the  corneo-scleral  or 
scleral  one  as  yet  only  partly,  or  not  at  all  closed.  In  conse- 
quence of  the  peculiar  structure  of  the  conjunctival  tissue 


58  THE  HUMAN  EYE. 

with  its  network  of  open  canals,  the  fluids  coming  from  the 
cornea  and  anterior  chamber  can,  of  course,  easily  escape  into 
it.  Histologically  we  find  only  the  meshes  filled  with  lym- 
phatic fluid,  and  more  or  less  distended. 

Similar  conditions  are  found  in  cases  of  so-called  sub- 
conjunctival haemorrhage.  Whether  such  a  haemorrhage  was 
caused  by  an  injury  or  came  on  spontaneously,  we  simply  find 
the  meshes  and  canals  of  the  conjunctival  tissue  filled  with 
blood  and  distended.  The  blood  gradually  becomes  absorbed, 
and  leaves,  only  in  rare  cases,  some  pigment  behind.  It  is  very 
probable,  but  as  yet  not  proven  by  histological  examination, 
that  pathological  alterations  in  the  walls  of  the  conjunctival 
blood-vessels  give  rise  to  these  haemorrhages. 

A.  Conjunctivitis  (of  the  Conjunctiva  Bulbi)  and  its 

Results. 

When  examining  into  the  different  forms  of  inflammation 
of  the  conjunctiva  bulbi,  we  find  the  same  forms  we  meet 
with  in  other  mucous  membranes,  viz.,  catarrhal,  blennorr- 
hoic,  croupous  and  diphtheritic  conjunctivitis.  Such  an  in- 
flammation of  the  conjunctiva  bulbi  is  nearly  always  only 
a  symptom  of  inflammation  of  the  whole  conjunctiva.  This 
is,  however,  not  the  case  with  two  types  of  inflammation 
which  are  not  among  those  just  enumerated,  viz.,  phlyc- 
tenular conjunctivitis  and  clinically  so-called  episcleritis,  which 
are,  as  a  rule,  local  diseases.  A  farther  form  of  inflammation, 
but  rarely  observed  in  the  conjunctiva  bulbi,  is  trachoma. 

a.  Conjunctivitis  Catarrhalis,  Episcleritis,  PklyctcB?iula. 

Catarrhal  inflammation  of  the  conjunctiva  bulbi  is  ob- 
served only  when  the  whole  of  the  conjunctiva  is  subject  to 
a  catarrhal  inflammation.  The  blood-vessels  in  such  cases  are 
very  hyperaemic.  Thus  an  increased  transudation,  at  first  of 
the  serous  fluid  of  the  blood,  and  later  of  white  blood-corpu- 
scles into  the  meshes  of  the  conjunctival  tissue  is  caused,  which 
is  accompanied  by  an  increased  secretion  from  the  mucous- 
cells.  This  condition  can  heal  perfectly  by  removal  of  the 
hyper-secretion  from  the  conjunctival  surface  and  by  ab- 
sorption, or  it  may  become  chronic.     In  rare  cases  new-forma- 


CONJUNCTIVA  BULBI  AND  EPISCLERAL  TISSUE.         59 

tion  of  connective-tissue   in   the  conjunctiva  may  take  place 
during  the  process  of  such  a  chronic  catarrhal  conjunctivitis. 

The  disturbances  in  the  circulation  caused  by  the  considera- 
ble degree  of  hyperaemia  always  found  incases  of  conjunctivi- 
tis, may  also  lead  to  affections  of  the  cornea,  or,  as  is  frequently 
the  case,  to  hyperaemia  of  the  iris.  While  the  latter  is  often 
found  complicating  with  an  acute  catarrhal  conjunctivitis,  the 
former  affections  result  more  frequently  from  a  chronic  one. 

Clinicists  make  a  distinction  between  catarrhal  conjunc- 
tivitis and  episcleritis.  They  maintain  that  in  the  latter  the 
conjunctival  tissue  nearest  to  the  sclerotic  is  the  seat  of  the  in- 
flammation. As  far  as  I  know,  cases  of  such  clinically  diag- 
nosticated episcleritis  have  not  yet  been  examined  with  the 
microscope.  Where  episcleritis  is  a  primary  disease  (and  not 
secondary  to  inflammation  of  the  sclerotic,  etc.),  it  is,  as  a  rule, 
a  local  and  very  chronic  affection.  In  rare  cases  it  may  travel 
all  around  the  cornea  and  cause  internal  complications,  such 
iritis  is,  choroiditis,  and  even  neuro-retinitis.  Episcleritis  is 
always  accompanied  by  a  local  catarrhal  conjunctivitis,  and 
there  is  probably  no  catarrhal  conjunctivitis  of  a  more  serious 
degree  which  is  not  combined  with,  or  causes  some  degree  of 
episcleritis. 

Another  local  form  of  inflammation  of  the  conjunctiva, 
which  is,  however,  as  a  rule,  combined  with  a  local,  often  even 
with  a  general  catarrhal  conjunctivitis,  is  phlyctenula. 

As  far  as  I  know,  phlyctenula  of  the  conjunctiva  have 
not  yet  been  histologically  examined.  The  process  is  clini- 
cally, however,  so  similar  to  that  in  the  cornea,  that  we 
shall  probably  not  be  very  far  from  the  truth  in  assuming 
that  we  here  also  find  a  sub-epithelial  infiltration  with  round 
cells.  This  infiltration  may  later  on,  be  again  absorbed,  or 
lead  to  the  destruction  of  the  epithelium  above  it,  and  thus 
cause  the  formation  of  a  superficial  ulcer.  The  phlyctenula 
may  appear  singly  or  we  may  find  a  number  at  the  same  time. 
A  variety  of  this  affection  is  the  so-called  miliary  phlyctenula. 

b.  Conjunctivitis  Blejtnorrhoica  {purulenta,  gonorrhoica),  Ulcer 
of  the  Conjunctiva. 

In  blennorrhoic  conjunctivitis,  the  characteristic  secretion 


6o  THE  HUMAN  E  YE. 

is  at  first  muco-purulent,  later  on,  entirely  purulent.  Blennorr- 
hoic  conjunctivitis  of  the  conjunctiva  bulbi  is  nearly  always 
caused  by  an  inflammation  of  the  same  nature  of  the  whole 
conjunctiva,  and  probably  always  combined  with  an  inflam- 
mation of  the  episcleral  tissue. 

The  conjunctival  blood-vessels  are,  in  these  cases,  always 
highly  hyperaemic,  and  this  hyperaemia  is  followed  by  the 
emigration  and  new-formation  of  numerous  round-cells. 
These  symptoms  are  combined  with  oedema  and  swelling  of 
the  conjunctiva,  which  again  cause  stasis  in  the  veinous  blood- 
vessels and  passive  oedema,  and  thus  a  circuliis  vitiosus  is 
formed.  The  infiltration  and  new-formation  of  round-cells 
are  followed  by  a  lively  proliferation  of  the  epithelial  cells, 
and  it  seems  later  they  not  only  allow  the  pus-cells  to  pass 
through  them,  but  themselves  take  an  active  part  in  the 
formation  of  the  pus.  During  this  process  small  superficial 
ulcers  are  frequently  formed.  Such  small  ulcers  heal  by 
proliferation  of  the  surrounding  epithelium,  and  it  seems  that 
all  the  layers  take  an  active  part  in  this  restorative  process. 
The  same  healing-process,  combined  with  a  local  blennorrhoic 
conjunctivitis,  is  observed  after  the  breaking  of  the  pustule 
formed  by  a  phlyctenula. 

After  having  lasted  some  time,  blennorrhoic  conjunctivitis 
generally  goes  over  into  the  catarrhal  form,  which  may  soon 
lead  to  the  normal  condition  or  become  chronic.  Such  a 
chronic  catarrhal  conjunctivitis  after  blennorrhoea  often  pro- 
duces trachoma. 

Serious  cases  of  blennorrhoea  of  the  conjunctiva  are  nearly 
without  exception  combined  with  inflammatory  processes  in 
the  cornea,  which  may  lead  to  partial  or  total  destruction  of 
this  membrane,  or  even  of  the  whole  eye-ball.  It  is  as  yet 
an  unsettled  question  whether  these  complications  originate 
in  an  inoculation  of  pus-cells  into  the  corneal-tissue,  or  only 
in  impaired  nutrition,  or  in  both  combined.  It  seems  to  me, 
however,  that  the  latter  is  the  most  probable. 

As  a  result  of  blennorrhoic  conjunctivitis  (especially  when 
combined  with  ulcus  corneae),  we  find  the  formation  of  ptery- 
gium, as  I  have  already  above  stated. 

The  swelling  of  the  papillae,  which  is  so  conspicuous  in  the 


CONJUNCTIVA  BULBI  AND  EPISCLERAL    TISSUE.       6 1 

conjunctiva  of  the  lids,  in  cases  of  blennorrhoea,  is  not  ob- 
served in  the  conjunctiva  of  the  bulbus,  since,  as  stated,  it  has 
no  papillae. 

c.   Conjunctivitis  Crouposa  and  Diphtheritica. 

Although  these  two  forms  of  conjunctivitis  do  not  seem 
to  have  been  as  yet  histologically  examined,  their  analogy 
with  the  same  forms  of  inflammation  in  other  mucous  mem- 
branes will  help  to  explain  the  conditions.  We  therefore 
probably  find  in  croupous  conjunctivitis  that  a  fibrino-puru- 
lent  exudation  is  deposited  upon  the  surface  of  the  conjunc- 
tiva, without  implicating  the  epithelial  layer.  Croupous 
membranes,  taken  from  the  conjunctiva,  consist  invariably 
of  a  dense  network  of  fibrinous  threads,  among  which  round- 
cells  lie  in  large  quantity.  The  same  exudation  is  probably 
found  in  diphtheritic  conjunctivitis ;  but  here  it  materially 
involves  the  epithelium  and  the  underlying  tissue.  The 
croupous  exudation,  therefore,  when  cast  off,  leaves  only  an 
inflamed  conjunctiva  behind,  while  the  diphtheritic  membrane 
is  never  cast  off  without  causing  a  deep  ulcer. 

The  croupous  as  well  as  the  diphtheritic  form  of  inflamma- 
tion are  only  rarely  found  to  involve  the  bulbar  conjunctiva. 
When  healing  they  go  over  into  a  blennorrhoic,  and  this  later 
on  into  a  catarrhal  conjunctivitis,  which  may  either  soon  lead 
to  the  normal  condition  or  become  chronic.  In  the  latter  case 
they  may,  too,  produce  trachoma. 

Both  these  kinds  of  conjunctivitis  often  result  in  destruc- 
tion of  the  cornea,  or  even  of  the  whole  eye-ball. 

d.  Conjunctivitis  Trachomatosa. 
Although  trachoma  is  frequently  the  result  of  chronic 
catarrhal,  blennorrhoic,  or  in  some  cases  croupous  and  diph- 
theritic conjunctivitis,  it  is  also  observed  as  a  primary  dis- 
ease. It  is  only  found  in  the  bulbar  conjunctiva,  after  it  has 
affected  the  whole  of  the  remaining  conjunctiva.  My  own 
examinations  of  trachomatous  conjunctiva  have  taught  me 
that  its  characteristic  feature  is  the  formation  of  tubercle-like 
aggregations  of  round-cells.  These  clusters  of  round-cells  are 
more  or  less  globe-shaped,  and  force  the  surrounding  tissue 
(which  is  also  filled  with  round-cells;  aside,  at  the  same  time 


62 


THE  HUMAN  E  YE. 


compressing  its  fibres  in  such  a  way,  that  a  number  of  authors 
thought  the  granules  were  surrounded  by  a  membrana  pro- 
pria, and  were  hypertrophic  lymph-folHcles.  But  there  are  no 
lymph-follicles  in  the  human  bulbar  conjunctiva,  and  the  ap- 
parent membrana  propria  is,  as  stated,  formed  by  the  com- 
pressed fibres  of  the  conjunctival  tissue.  If  the  blood-ves- 
sels of  the  conjunctiva  are  injected  with  some  tinted  fluid,  it 

Co 


Fig.  24. — Trachoma-granule  from  the  bulbar  conjunctiva.     Blood-vessels  injected  with  a 
stained  fluid.     L.  Enlarged  lymph-canals. 

is  easily  seen  that  they  pass  through  these  accumulations  of 
round-cells.  (See  Fig.  24.)  Besides  the  blood-vessels,  I  always 
found  enlarged  lymphatic  vessels  in  and  around  the  granules. 

These  granules  may  reach  the  corneo-scleral  margin,  and 
sometimes  they  are  even  found  to  lie  in  the  corneal  tissue 
near  this  place. 

Trachomatous  conjunctivitis  is  usually  a  chronic  affection, 
and  produces  a  hyper-secretion  of  mucous,  or  the  secretion 
of  a  muco-purulent  fluid.  The  granules  may  undergo  fatty 
degeneration,  and  thus  be  absorbed,  or  they  are  transformed 
into  a  tough  connective-tissue  {Preuss).  This  new-formed 
tissue  causes  the  obliteration  of  blood-vessels  and  lymph 
canals  and  destruction  of  the  mucous-cells.  The  latter 
leads  to  xerosis  of  the  cornea.  Corneal  affections  are,  more- 
over, very  frequent  complications  in  cases  of  trachomatous 
conjunctivitis.  It  produces,  however,  comparatively  seldom 
internal  affections  or  the  perfect  destruction  Df  the  eye-ball. 

The  Results  of  Conjunctivitis,  viz.,  Argyrosis,  Xerosis,  and 

Pterygium. 
Argyrosis  of  the  conjunctiva  is  not  caused  by  the  con- 


CONJUNCTIVA  BULB!  AND  EPISCLERAL   TISSUE.       g^ 

junctivitis  itself,  but  by  a  too  prolonged  use  of  the  chief  rem- 
edy employed  in  its  treatment — nitrate  of  silver.  This  condi- 
tion, according  to  Jiinge,  is  due  to  the  precipitation  of  the 
silver  in  the  epithelium  and  the  superficial  layers  of  the  con- 
junctival tissue. 

Xerosis  conjunctivae  we  call  an  affection  which  is  caused 
by  the  dryness  of  the  conjunctiva  and  the  transformation  of 
its  epithelial  cells  into  horny  scales.  This  process  may  be 
combined  with  the  formation  of  scar-tissue  in  the  conjunctiva 
or  exist  without  it  (xerosis  parenchymatosa  and  xerosis  sim- 
plex), and  originates  in  a  want  of  moisture  dependant  upon 
chronic  forms  of  conjunctivitis,  especially  trachoma.  The 
mucous-cells  are  found  either  undergoing  a  colloid  metamor- 
phosis or  altogether  destroyed.  Xerosis  conjunctivae  is 
generally  accompanied  by  the  same  affection  of  the  cornea. 

Pterygium,  as  stated  above,  may  originate  in  a  marginal 
ulcer  of  the  cornea,  combined  with  blennorrhoic  conjunctiv- 
itis. I  have,  however,  learned  by  clinical  observation  that 
it  may  just  as  well  be  caused  by  catarrhal  conjunctivitis 
(especially  in  the  acute  form),  without  the  existence  of  an 
ulcer. 

B.  Injuries  to  the  Conjunctiva  and  their  Results. 

I .  Injuries  zvithout  the  Retention  of  a  Foreign  Body. 

Injuries  to  the  conjunctiva,  without  retention  of  a  foreign 
body,  ^re  either  cuts,  rents  or  scratched  wounds.  The  cuts 
we  observe  on  the  bulbar  conjunctiva  are  chiefly  those  caused 
by  an  operation.  If  the  tissue  has  simply  been  severed  heal- 
ing by  primary  intention,  generally  takes  place  and  no  trace 
is  left  behind.  If  the  cut,  however,  causes  a  loss  of  sub- 
stance, or  for  some  reason  the  wound-lips  are  not  allowed  to 
become  well  applied  to  each  other,  the  healing  process  occurs 
by  secondary  intention.  We  then  find,  similar  to  those  condi- 
tions seen  after  a  corneal  wound,  an  exudation  of  a  fibrinous 
nature  covering  the  loss  of  substance,  or  between  the  wound- 
lips,  which  is  gradually  transformed  into  connective-tissue, 
and  then  covered  by  new-formed  epithelium.  In  the  new- 
formation  of  the  latter,  all  the  layers  seem  to  participate. 


64 


THE  HUMAN  E  YE. 


If  the  wound  lies  at  the  corneo-scleral  margin,  it  is,  as  stated 
above,  covered  to  the  larger  extent  by  the  conjunctival,  to 
the  smaller  by  the  corneal  epithelium. 

2.    Wounds  with  Subsequent  Retention  of  a  Foreign  Body. 

If  a  foreign  body  remains  in  the  conjunctiva  after  having 
pierced  only  the  epithelium  and  the  layers  under  it,  it  nearly 
always  produces  a  general  catarrhal  and  a  local  blennorrhoic 
conjunctivitis.  The  latter  leads  to  the  formation  of  an  ulcer 
around  the  foreign  body,  which  then  is  thrown  off  with  the 
pus,  and  the  ulcer  heals  in  the  usual  way. 

If  the  foreign  body  has  entered  the  deeper  layers  of  the 
conjunctiva,  and  is  small  enough  to  remain  embedded  there, 
it  is  usually  soon  surrounded  by  dense  connective-tissue 
capsule,  which  is  the  result  of  chronic  conjunctivitis.  Among 
such  foreign  bodies  we  find  little  pieces  of  wood,  iron  or  stone. 


Fig.  25.  Crystalline  lens  dislocated  under  the  conjunctiva  and  there  encapsuled. 

Lenses  dislocated  under  the  bulbar  conjunctiva  produce  the 
same  results.     (See  Fig.  25.) 

3.  Burns  with  Lime. 

Burns  of  the  conjunctiva,  like  those  of  the  cornea,  are 
mostly  caused  by  lime.  The  epithelial  cells  and  the  under- 
lying tissue  are  infiltrated  with  the  lime,  become  necrotic, 
and  then  acting  as  foreign  bodies,  produce  a  local  blen- 
norrhoic conjunctivitis,  besides  the  general  catarrhal  conjunc- 
tivitis. Thus  the  burned  parts  are  thrown  off,  and  an  ulcer 
is  formed  which  heals  in  the  manner  described. 


CONJUNCTIVA  BULBI  AND  EPISCLERAL   TISSUE.       65 

If  the  conjunctiva  of  the  lids  has  been  burned  at  the  same 
time  and  the  two  ulcers  lie  close  to  each  other,  their  surface 
may  heal  together.  This  condition  is  called  symblepharon 
posterius.  If  the  burn  be  extensive  enough,  it  may  cause 
the  formation  of  an  anchyloblepharon. 

C.  Tumors  of  the  Conjunctiva  Bulbi  and  Episcleral 

TISSUE. 

In  chapters  I  and  II,  I  remarked  that  the  so-called  tumors 
of  the  cornea  and  sclerotic  as  a  rule,  take  their  origin  from 
the  limbus  conjunctivae,  which  is  so  well  supplied  with  blood- 
vessels, and  not  from  either  cornea  or  sclerotic.  The  litera- 
ture on  this  subject  and  the  clinical  experience  of  others  as 
well  as  my  own  numerous  histological  examinations  have 
thoroughly  convinced  me  that  no  genuine  corneal  or  scleral 
tumors  are  observed,  at  least,  that  no  tumor  has  so  far  been 
described  which  undoubtedly  took  its  origin  in  either  the 
cornea  or  the  sclerotic  alone.  I  have  therefore  thought  it 
proper  to  place  the  description  of  all  these  tumors  here. 

Metastatic  tumors  in  these  parts,  resulting  from  intra- 
ocular new-formations,  do  not  of  course,  belong  under  this 
head. 

a.  Lymphangiectasia  and  Serous  Cysts. 

I  am  not  aware  that  the  result  of  a  histological  examina- 
tion of  a  lymphangiectasia  of  the  conjunctiva  has  ever  been 
published  before  the  following  one  which  I  had  occasion  to 
examine  and  to  describe  in  my  paper  on  the  nature  and  ana- 
tomical causes  of  sympathetic  ophthalmia.  The  conditions 
were,  as  follows  ; 

In  the  conjunctiva  bulbi  I  found  a  system  of  cavities  and 
canals,  perfectly  independant  of  the  blood-vessels,  which  were 
hyperaemic  and  therefore  well  defined.  These  cavities  and 
canals  are  in  direct  communication  with  each  other,  and  press 
the  surrounding  conjunctival  tissue  aside.  Some  of  them 
are  separated  from  each  other  only  by  a  very  thin  septum. 
They  contain  a  serous  fluid,  in  which  a  small  number  of  lym- 
phatic cells  are  suspended.  Their  walls  have  an  endothelial 
lining  which,  however,  does  not  seem  to  be  continuous.     The 


66 


THE  HUMAN  E  YE. 


walls  themselves  are  formed  by  the  compressed  fibres  of  the 
conjunctival  tissue  (See  Fig.  26). 


Kio.  26.   Lymphangiectasia  of  the  bulbar  conjunctiva. 

If  the  ectasia  of  such  lymph-canals  increases  still  further 
and  the  septa  disappear  altogether,  all  the  different  small 
cavities  may  coalesce  into  one  large  one  and  form  a  serous 
cyst.  That  serous  cysts  acquired  after  birth  may  be  devel- 
oped in  such  a  way,  has  also  been  stated  by  clinical  observers 
{School,  von  Wixker). 

I  have  had  no  occasion  to  examine  congenital,  uncompli- 
cated serous  and  dermoid  cysts  of  the  conjunctiva. 

b.  Granuloma  {Polypus). 


Granuloma  of  the  conjunctiva  is  but  seldom  observed 
upon  the  bulbar  part  of  this  membrane.  It  is  caused  by 
chronic  inflammatory  processes,  or  by  traumatic  and  opera- 
tive influences.  In  cases  where  the  eye-ball  is  phthisical,  it 
appears  sometimes,  as  if  the  granuloma  had  originated  in  the 
corneal  tissue,  which  is,  however,  not  the  case.  According 
to  my  experience,  there  exists  no  granuloma  of  the  cornea, 
although  Pagenstecher  and  Geuth  have  described  such  a 
tumor.  If  the  eye  is  as  yet  a  useful  organ  granulomata 
are  seldom  allowed  to  grow  to  a  considerable  size  but  are  re- 
moved at  an  early  stage.  Upon  phthisical  (blind)  eye-balls 
these  tumors  sometimes  grow  very  large.  All  the  tumors  be- 
longing under  this  head  and  examined  by  me,  were  built  up  of 
simple  granulation-tissue,  viz.,  round-cells,  new-formed  blood- 
vessels and  very  little,  if  any,  connective-tissue  (See  Fig.  27). 


CONJUNCTIVA  BULBI  AND  EPISCLERAL   TISSUE.       67 

Fano's  decription  of  a  "  fibrous  "  polypus  in  this  region,  may 
be  taken  as  a  proof  that  this  granuloma-tissue  may  later  on 


Fig.  37.  Granuloma  (polypus)  of  the  bulbar  conjunctiva 

become  transformed  into  dense  connective-tissue.  Mucoid 
polypi  {Saemisch)  have  never  come  under  my  observation  in 
this  part  of  the  eye. 

c.  Dermoid  and  Lipomatous  Tumors. 

Dermoid  (Rybd)  tumors  of  the  conjunctiva  are,  it  seems, 
always  independent  new-formations.  In  all  of  the  cases  hith- 
erto described  the  tumor  was  situated  just  upon  the  corneo- 
scleral margin  in  such  a  way,  that  one  half  was  adherent  to  the 
cornea,  while  the  remaining  half  lay  upon  the  sclerotic.  All 
authors  agree  as  to  the  benign  character  of  these  tumors,  and 
all  describe  them  as  consisting  of  the  constituents  of  the  normal 
skin.  In  rare  cases  in  the  latter  periods  of  life  dermoid  tumors 
through  some  cause  or  other  may  become  irritated  and  begin 
to  grow.  They  are  then,  of  course,  with  regard  to  the  useful- 
ness of  the  eye  of  a  malignant  character.  In  a  very  large  major- 
ity of  the  cases,  however,  dermoid  tumors  remain  stationary. 

The  histological  appearance  of  three,  such  new-formations 
which  I  myself  had  occasion  to  examine  is  described  in  the 
following.     (See  Fig.  28). 

The  dermoid  tumor  is  covered  with  a  continuous  epithe- 
lial coat,  which  consists  of  the  same  layers  and  elements  as 
the  epidermis.  The  most  superficial  layer  is  formed  by  flat- 
tened epithelial  cells,  which,  however,  are  not  always  horny. 
Cells  undergoing  colloid  metamorphosis  seem  to  be  frequent 
in  this  layer.  The  layer  under  the  flattened  cells  has  well 
marked  serrated  cells.     Mucous-cells  as  they  are  found  in  the 


6S  THE  HUMAN  E  YE. 

conjunctiva,  are  also  found  among  the  epithelial  cells  of  der- 
moid tumors.     This  epithelial  coat  has  as  uneven  a  surface 


Fig.  28. — Dermoid  tumor  of  the  bulbar  conjunctiva. 

as  that  of  the  skin,  and  sends  numerous  offsets  into  the  un- 
derlying tissue  surrounding  the  papillae  of  the  tumor.  In 
nearly  all  of  these  indentations,  we  find  a  hair  or  the  orifice 
of  a  gland.  The  latter  are  of  the  acinous  type  and  probably 
all  sudoriferous.  The  hairs  are  very  thin  and  have  very  little 
pigment.  Under  the  epithelium  lies  the  connective-tissue, 
which  appears  very  tough  and  dense,  and  contains  a  few  elastic 
fibrillae.  At  the  base  of  the  tumor  the  connective-tissue,  be- 
comes looser  and  includes  a  varying  amount  of  fat  cells.  It 
seems  thus  far  only  tumors,  which  had  been  removed  from  the 
globe  have  been  subjected  to  anatomical  examination, and  that 
their  basis  is  always  found  to  consist  chiefly  of  subcutaneous 
fat-tissue.  In  other  tumors  the  fat-tissue  may  form  the  bulk 
of  the  tissue,  and  such  tumors  have  by  several  authors  been 
described  as  lipomatous  dermoid  tumors.  Purely  lipomatous 
tumors  of  this  part  have  also  been  spoken  of  by  some  authors, 
but  I  am  inclined  to  think  that  they  were  actually  dermoid 
with  a  large  amount  of  fat-tissue. 

It  has  been  stated  by  others  that  most  of  the  dermoid  tu- 
mors contain  only  very  few  blood-vessels.  In  the  three  cases 
which  I  examined,  the  blood-vessels  were  as  numerous  as  in 
the  skin  and  the  network  of  capillaries  in  the  papillae  was 
especially  well  developed.  Nerves  have  not  been  found  in 
these  tumors,  which,  however,  does  not  altogether  prove  that 
they  really  do  not  exist. 

In  one  of  my  own  cases,  I  found  the  connective-tissue 
which  lay  directly  under  the  epithelium,  filled  with  round- 


CONJUNCTIVA  BULBI  AND  EPISCLERAL  TISSUE.        69 

cells  and  the  blood-vessels  were  very  hyperaemic.  I  think  that 
this  dermoid  tumor  was  in  a  state  of  irritation  that  would 
have  enabled  it  to  grow. 

The  connection  between  these  tumors  and  the  under-lying 
tissues  has,  as  far  as  I  know,  not  yet  been  described,  as  all 
the  published  cases  concerned  dermoid  tumors  which  were 
removed  from  the  living  eye-ball.  From  clinical  observation 
we  know,  however,  that  while  they  are  only  loosely  connected 
with  the  conjunctiva  (resp.  sclerotic),  they  adhere  firmly  to 
the  cornea. 

d.  Fibroma  and  Osteoma. 

Fibroma  and  osteoma  of  the  bulbar  conjunctiva  have  but 
seldom  been  observed. 

A  fibroma  described  by  Saemisch  was  found  upon  the  pos- 
terior part  of  the  bulbar  conjunctiva.  It  consisted  of  dense 
connective-tissue  with  a  few  cells.  The  latter  showed  all  the 
stages  of  development  of  a  cell  into  connective-tissue  fibre. 

Osteoma  {yon  Graefe,  Saemisch)  was  found  to  be  lying  in 
a  capsule  of  tough  connective-tissue  and  to  be  true  osseous 
tissue.  Watson  described  an  osteoma  in  the  conjunctiva  as 
springing  directly  from  the  sclerotic. 

e.  Papilloma,  melanoma  and  melanocancroid  new -formations. 

Among  the  benign  tumors  of  the  bulbar  conjunctiva 
papilloma  and  melanoma  have  been  described. 

Skokalsky  s  case  of  papilloma  corneae  is  the  only  one 
which  has  been  carefully  studied,  and  seems  to  allow  of 
no  doubt  as  to  the  diagnosis.  {Horner  s  case  of  a  "  fibroma 
papillare  "  will  be  mentioned  later  on).  The  description  clearly 
shows,  however,  that  this  case,  too,  was  not  a  corneal  tumor, 
but  sprang  from  the  corneo-scleral  margin,  that  is,  from  the 
conjunctival  or  episcleral  tissue.  It  formed,  cauliflower-like,  a 
number  of  cylindrical  excrescences  which  consisted  of  spindle- 
cells,  containing  blood-vessels,  and  was  covered  with  epi- 
thelium. 

The  "  pure  "  melanoma  is  generally  described  as  a  benign 
tumor.     The  benign  character  seems,  however,  very  doubtful, 


70 


THE  HUMAN  E  YE. 


as  most  of  authors,  including  Scemisch,  report  that  at  any  time 
it  may  become  malignant.  The  anatomical  conditions  of  me- 
lanoma of  the  conjunctiva  generally  mentioned  do  not  ap- 
pear to  warrant  its  being  called  a  distinct  species  of  new-forma- 
tion. Such  a  melanoma  described  by  Heddaeus  and  taken  from 
the  corneo-scleral  margin,  consisted  of  "  detritus,  epithelial 
cells  with  and  without  pigment,  free  nuclei,  free  pigment, 
numerous  large  round  cells  with  large  nuclei  and  nucleoli." 
Probably  most  of  these  tumors  belong  to  the  sarcomata. 

Once  only  I  had  myself  the  opportunity  to  examine  such 
a  tumor,  which  had  been  removed  from  the  conjunctiva  as  a 
benign  melanoma,  and  I  found  the  following  conditions. 

On  the  whole  the  new-formati*on  was  very  much  like  that 
of  a  dermoid  tumor.  Under  a  thick  layer  of  epithelium  came 
first  connective-tissue  with  numerous,  then  one  with  scarcely 
any  cells,  and  the  base  of  the  tumors  was  formed  by  a  loose 
tissue  containing  fat-cells.  The  blood-vessels  were  very 
numerous  and  they  formed  papillae  like  those  found  in  the 
skin. 

The  epithelium  however,  had  several  remarkable  pecu- 
liarities. (See  Fig.  29.)  From  the  epithelial  layer  large  pa- 
pillae spring  forward  like  pointed  condylomata,  and  these  ep- 
ithelial papillae  contain  cavities  and  small  canals  which  can 
sometimes  be  traced  to  the  lymphatic  vessels  in  the  tissue 
underneath  the  epithelium.  The  epithelial  cells  bordering 
these  cavities  and  those  at  the  base  and  top  of  the  papillae 
are  pigmented  to  a  varying  degree.  The  granular  pigment 
lies  in  the  protoplasma  of  the  cells  as  well  as  in  the  cement- 
ing substance  between  them.  The  inner  layers  of  the  epithe- 
lium consist  of  well  defined  and  large  serrated  cells.  The 
nearer  the  surface  the  more  they  go  over  into  flattened  epi- 
thelial cells  and  horny  scales.  Some  of  the  papillae  show 
pearl-nodules. 

Furthermore,  the  tumor  contains  glands  and  hair.  The 
hairs  are  very  thin,  only  slightly  pigmented  and  two  of  them 
generally  stand  together.  The  glands  are  very  much  like  the 
Meibomian  glands  in  the  lids  but  I  do  not  know  their  exact 
nature.     A  strong  nerve-branch  enters  the  base  of  the  tumor. 

The  question  now  is,  what  is  the  anatomical  diagnosis  of 


CONJUNCTIVA  BULBI  AND  EPISCLERAL   TISSUE.-      71 

this  "  melanoma  "  ?     In  the  whole  of  its  structure  the  growth 
throughout  most  resembles  a  dermoid  tumor,  with  the  differ- 


FiG.  29. — Partially  pigmented  epithelial  papilte  from  a  dermoid   tumor  of  the   bulbar 
conjunctiva. 

ence  that  it  has  papillary  and  epithelial  excrescences.  There 
are,  however  a  great  number  of  pigmented  cells,  among  the 
latter  which  may  have  led  to  the  clinical  diagnosis  of  mel- 
anoma. Those,  however,  who  consider  pearl-nodules  as  a 
sure  characteristic  feature  of  an  epithelioma,  will  perhaps  call 
it  a  melano-cancroid. 

I  consider  it  to  be  a  peculiar  variety  of  the  dermoid  tumor 
and,  perhaps,  some  of  the  new-formations  described  as  mel- 
anomatous  and  melano-cancroid  tumors  may  belong  among 
the  same  class.  Some  of  them  were  undoubtedly  cases  of 
melanosarcomatous  tumors. 


f.  Leiicosarconia  and  Melanosarcoma. 
Sarcomata  of  the  episcleral  region  are  comparatively  rare, 
and  among  them  the  leucosarcomata  are  but  very  seldom 
found,  therefore,  the  number  of  these   new-formations  de- 
scribed in  literature  is  but  very  small. 


J2  THE  HUMAN  E  YE. 

Only  one  case  of  leucosarcoma  of  the  episcleral  region  has 
come  under  my  own  observation.  The  tumor  had  about  the 
size  of  a  pea  and  consisted  of  large  round,  mingled  with  a 
few  spindle-cells.  A  great  number  of  these  round-cells  had 
more  than  one  nucleus.  Furthermore,  I  found  among  them 
a  larger  number  of  giant-cells.  The  new-formation  contained 
a  great  many  blood-vessels,  lifted  the  conjunctival  and 
corneal  epithelium  off  the  underlying  parts  and  thus  grew  in 
between  Bowmatis  layer  and  the  corneal  epithelium,  without, 
however,  materially  altering  the  tissue  of  the  cornea. 

Later  on  the  elements  of  the  tumor  enter  the  sclerotic  and 
cornea  proper  {Pagenstecher  and  GentJi).  Hirschberg  de- 
scribed such  a  case  of  a  leucosarcoma  of  the  conjunctiva  with 
intra-ocular  metastases.  In  what  way  the  tumor  reaches  the 
inner  membranes  does  not  seem  to  be  known. 

Melanosarcomata  of  the  conjunctiva  have  been  observed 
and  histologically  examined  more  frequently  than  leucosar- 
comata.  All  authors  agree  in  the  prominently  vascular 
character  of  these  new-formations.  In  the  beginning  stages 
they  were  always  found  to  be  very  easily  separated  from  the 
underlying  tissue,  especially  from  the  cornea.  Very  fre- 
quently an  injury  to  the  eye-ball  has  to  be  considered,  as  the 
origin  of  the  sarcoma,  and  it  is  therefore  not  improbable,  that 
the  hemorrhage  caused  by  the  injury  has  something  to  do  with 
the  formation  of  the  pigment. 

I  have  examined  three  such  melanosarcomatous  tumors 
of  the  conjunctiva,  myself,  and  the  conditions  were  very 
much  alike  in  all  of  them. 

The  new-formation  seems  to  always  start  in  the  vascu- 
lar limbus  conjunctivae,  to  gradually  spread  between  the 
corneal  epithelium  and  Boivmans  layer,  until  at  a  certain 
stage,  it  is  found  to  lie  upon  the  cornea,  like  "  pannous-tissue  " 
without  as  yet  having  changed  this  membrane  at  all.  Later 
on,  however,  the  periphery  oi Bowman  s  layer  is  destroyed  and 
the  elements  of  the  new-formation,  enter  the  parenchyma  of 
the  cornea.  Bowman  s  layer  is,  however,  so  resistant,  that 
the  elements  of  the  tumor  when  they  have  once  entered  the 
corneal  parenchyma  progress  much  quicker  towards  the  cen- 
tre than  Bowman  s  layer  is  destroyed.     It  is  even  possible 


CONJUNCTIVA  BULBI  AND  EPISCLERAL    TISSUE.       73 

for  the  new-formation  to  encircle  the  whole  of  the  cornea, 
before  it  can  pierce  this  layer,  and  thus  grow  into  the  deeper 
parts. 

The  elements  of  melanosarcomata,  are  round  or  spindle- 
cells,  which  vary  considerably,  with  regard  to  the  amount 
of  pigment  they  contain.  We  find,  therefore,  in  one  and 
the  same  tumor,  parts  which  are  nearly  unpigmented,  while 
in  other  parts  the  cells,  contain  so  much  pigment,  that  it 
is  utterly  impossible  to  recognize  their  nuclei.  It  seems 
from  my  specimens  that  the  highest  degree  of  pigmenta- 
tion is  always  found  in  the  cells  which  lie  nearest  to  the 
blood-vessels.  The  more  superficial  parts  are  generally  the 
least  pigmented  ones.  The  cells  are  generally  larger  than 
white  blood-cells  and  have  one  or  more  nuclei.  I  have  never 
found  any  giant-cells  in  these  tumors.     (See  Fig.  30). 


Fig.  30.— Melanosarcoma  of  the  bulbar  conjunctiva.  1.  Shows  how  the  pigmented  cells 
creep  along  the  blood-vessels  of  the  conjunctiva  and  upon  Bowman's  layer  under  the 
epithelium  of  the  cornea. 

Most  of  the  authors  on  this  subject,  mention  the  scarcity 
of  an  intercellular  substance.  In  my  cases,  too,  I  could  only 
clearly  demonstrate  the  intercellular  substance,  in  the  peri- 
pheral parts  of  the  tumor.  The  large  number  of  capillaries 
form  a  dense  network.  Besides  them  I  find  a  number  of  well 
distinguished  veinous  and  arterial  branches.  The  vascularity 
of  these  tumors  readily  explains  the  recent  and  old  haemor- 
rhages usually  found  therein. 

From  my  specimens  it  appears  that  in  the  progress  of  the 
tumor,  the  blood-vessels  play  an  important  part.     In  one  of 


74 


THE  HUMAN  E  YE. 


the  cases  I  found  in  the  part  of  the  episcleral  tissue,  which 
lay  diametrically  opposite  the  original  tumor  a  network  of 
pigmented  stripes.  Examining  this  part  with  a  higher  mag- 
nifying power  I  found  the  network  to  be  formed  by  blood- 
vessels, which  were  not  only  surrounded  by  a  sheath  of  pig- 
ment but  which  also  contained  pigment  molecules  within  their 
lumen.  The  progress  of  the  tumor  into  the  parenchyma  of 
the  cornea  or  sclerotic,  is  always  preceded  by  the  new-for- 
mation of  blood-vessels  and  the  emigration  and  proliferation 
of  cells.  Along  these  new-formed  blood-vessels  the  pig- 
mented elements  of  the  tumor,  are  then  seen  to  creep  into 
the  corneal  and  sclerotic  tissue  and  to  gradually  destroy  the  la- 
mellae of  these  membranes.  It  does  not  seem  to  be  known 
whether  such  new-formations  lead  later  on  to  rupture  of  the 
cornea,  or  whether  they  may  grow  into  the  interior  of  the 
eye-ball. 

The  periphery  of  the  tumor  in  the  tissues  so  involved,  is 
always  formed  by  the  well  known  zone  of  inflammation,  and 
their  surface  is  covered  with  the  conjunctival  or  corneal  epi- 
thelium. 

g.  Epithelioma. 

Epithelioma  is  the  most  frequently  observed,  of  all  the 
tumors  of  the  episcleral  tissue.  Consequently  it  has  already 
often  been  examined  and  described.  The  authors  on  this 
subject  {Althoff,  Classen,  Horner,  Knapp  and  others),  how- 
ever, disagree  in  their  opinions  upon  important  points  so 
much,  that  in  the  following  I  only  give  the  results  of  my 
own  examinations,  which  up  to  this  time  embrace  fourteen 
cases.  I  will  only  mention  here  that  a  tumor  described  by 
Horner  as  a  "fibroma  papillare"  belongs  most  probably  to 
the  same  class  of  tumors,  as  the  patient  died  from  carcinoma. 
Furthermore,  old  epitheliomata  of  the  conjunctiva,  very  fre- 
quently show  the  pupillary  form  known  under  the  name  of 
"cauliflower  ''-cancer. 

Epitheliomata  originate  in  a  true  hyperplasia  of  the  epi- 
thelial layer  of  the  conjunctiva,  whether  they  start  directly 
from  the  corneo-scleral  margin  or  from  a  place  somewhat  re- 
mote from  it.     It  usually  begins  just  where  Bowman  s  layer 


CONJUNCTIVA  BULBI  AND  EPISCLERAL   TISSUE.        y^ 

joins  the  conjunctiva,  and  where,  as  stated  above,  the  normal 
conjunctival  epithelium  dips  into  the  underlying  tissue  in  the 
shape  of  one  or  two  papillae.  It  seems  that  epithelioma  never 
originates  from  the  epithelium  of  the  cornea  proper. 

We  find,  in  the  beginning,  the  epithelial  layer  considerably 
thickened,  and  this  thickening  is  caused  by  an  abnormally 
increased  number  of  epithelial  cells.  It  is  in  this  stage  fur- 
thermore, impossible  to  recognize  the  normally  so  distinct 
layers  of  the  corneal  and  conjunctival  epithelium,  since  the 
cells  vary  considerably  in  shape  and  size.  In  most  cases 
nearly  the  whole  of  this  original  tumor  consists  of  serrated 
cells,  in  others  the  cells  are  flat  and  partially  horny.  Every 
cell  (except  the  horny  ones)  have  a  large  round  or  oval  nu- 
cleus and  several  nucleoli,  cells  with  two  or  more  nuclei  are 
very  rare.  If  the  tumor  progresses,  the  surrounding  conjunc- 
tiva becomes  hyperaemic  and  filled  with  cells,  while  the  cornea 
proper  remains  for  a  long  time  unaltered.  Gradually,  how- 
ever, new  blood-vessels  enter  the  cornea  or  sclerotic  and 
round-cells  begin  to  emigrate  in  their  tissue,  which  process 
is  followed  by  the  proliferation  of  their  fixed  cells.  Only 
then  the  elements  of  the  tumor  seem  to  be  able  to  perforate 
the  peripheral  parts  of  Bowman  s  layer  (as  in  cases  of  sar- 


FiG.  31.— Epithelioma  of  the  bulbar  conjunctiva. 

coma)  and  grow  into  cornea  and  sclerotic,  arranged  in  the 
well  known  characteristic  gland-like  and  cylindric  way.  (See 
Fig.  31),      Epithelioma  enters  the  hard  membranes  of  the 


^6  THE  HUMAX  EYE. 

eye-ball,  without  having  first  destroyed  the  peripheral  parts 
of  Botvuian  s  layer  ;  the  progress  of  the  destruction  of  this 
layer  however,  does  not  necessarily  go  pari  passu  with  the 
progress  of  the  tumor  in  the  corneal  iizsw^,  Descemei' s  mem- 
brane can  resist  much  longer  and  may  be  found  perfectly 
intact,  even  if  the  whole  of  the  corneal  parenchyma  is  taken 
up  by  the  new-formation. 

The  following  are  the  more  minute  histological  details  to 
be  observed  in  these  new-formations. 

If  the  surface  of  the  epitheliomatous  growth  is  ulcerated, 
the  conditions  are  altered  accordingly.  Where  no  such  ulcer- 
ation exists,  I  find  the  superficial  layer  of  the  tumor  to  con- 
sist of  flattened,  often  horny,  epithelial  elements.  Under 
these  layers  come  the  cells  of  the  new-formation,  varying  in 
size  and  shape  and  mostly  serrated,  and  they  dip  into  the 
underlying  parts  forming  the  well  known  cylinders.  These  are 
the  primary  epithelial  cylinders.  They  are  surrounded  by  a 
tissue  filled  with  blood-vessels  and  round-cells.  These  round- 
cells  frequently  lie  so  close  together,  that  their  form  is  altered 
by  the  pressure.  They,  too,  vary  in  size.  We  find  among  them 
free  nuclei,  cells  with  one  or  two,  and  larger  ones  with  even 
three  and  four  nuclei. 

The  outlines  of  these  primary  epithelial  cylinders  are 
mostly  sharply  defined  and  their  periphery  is  formed  by  a 
single  layer  of  cylindrical  or  cone-shaped  cells,  which  are  also 
frequently  serrated.  The  centre  of  the  cylinders,  consists  of 
epithelial  cells  of  very  different  size  and  shape  ;  pearl-nodules 
are  frequently  found  among  them. 

If  we  follow  up  such  primary  cylinders  under  the  micro- 
scope, we  see  that  some  of  them  have  a  blunt  end,  others 
branch  off  into  secondary  and  tertiary  cylinders  of  the  same 
kind,  while  others  again  pass  over  into  round-cell  cylinders, 
which  then  are  gradually  lost  in  the  surrounding  cellular 
tissue.  (See  Fig.32).  Although  Knapp  states  distinctly  that 
all  cylinders  consist  of  epithelial  cells  and  that  he  never  saw 
epithelial  cell  cylinders  go  over  into  round-cell  cylinders, 
my  own  specimens  all  show  this  condition  undoubtedly.  In 
some  specimens  I  found  even  large  networks  of  such  secon- 
dary and  tertiary  cylinders,  which  consist  solely  of  round-cells. 


CONJUNCTIVA  BULBI  AND  EPISCLERAL  TISSUE.       jj 

Sometimes  I  saw  a  number  of  epitheloid  cells  (which  are 
similar  to  epithelial  cells  in  shape,  and  like  them,  by  Muel- 
ler s   hardening  fluid   tinted   darker   than    the  surrounding 


/ 


Fig.  32. — Epithelioma  of  the  bulbar  conjunctiva,    i.  Epithelial  cylinder  filled  with  round- 
cells.    2.  Epithelial  cylinders  ending  in  round-cell  cylinders. 

tissue)  lying  just  in  the  angle  where  younger  cylinders 
branched  off  from  older  ones.  Although  I  was  never  able  to 
see  directly  the  transformation  of  round  into  epithelial  cells,  I 
could  not  explain  the  conditions,  without  assuming  that  such 
a  change  occurs.  This  seems  to  be  still  more  probable,  as  I 
frequently  found  also  round-cell  cylinders  whose  periphery 
was  formed  by  a  single  layer  of  epithelial  cells.  (See  Fig.  32). 
I  want  to  state  here,  furthermore,  that  while  the  round-cells 
very  distinctly  show  the  phenomena  of  proliferation,  the 
number  of  undoubtedly  proliferating  epithelial  cells,  is  but 
very  small. 

The  epithelial  cylinders  seem  in  the  beginning  to  grow 
along  the  corneal  canals  {Knapf).  Later  on,  however,  the 
condition  of  the  lamellae  becomes  changed  in  such  a  way, 
that  we  can  no  longer  speak  of  corneal  canals.  The  lamellae 
are  broken  up  and  destroyed.  We  then  find  the  cylinders 
surrounded  by  a  tissue,  consisting  of  very  fine  spindle-cells. 
(See  Fig.  33). 

When  the  tumor  has  grown  over  the  whole  cornea.  Bow- 
man s  layer  is  always  wanting.  During  the  growth  of  the 
tumor,  however,  this  layer  is  not  as  quickly  destroyed,  as  the 
elements  of  the  new-formation  spread  in  the  corneal  tissue. 
Descemefs  membrane,  which  as  stated  above,  resists  much 
longer,  may  in  consequence  of  ulceration  and  an  increased 


78 


THE  HUMAN  E  YE. 


intra-ocular  pressure,  at  a  later  period  be  also  perforated. 
When  this  perforation  takes  place  the  capsule  of  the  crystal- 
line lens  is  often  ruptured,  or  the  lens  may  escape  from  the 


Fig.  33. — Epithelioma  of  the  bulbar  conjunctiva.    The  tissue  of  the  cornea  is  changed  into 
one  consisting  of  long  fine  spindle-cells. 

eye-ball  in  toto.  When  the  perforation  occurs,  the  iris  prob- 
ably always  prolapses,  and  thus  becomes  adherent  to  the 
new-formation.  In  this  manner  one  channel  is  opened,  by 
which  the  elements  of  the  tumor  can  enter  the  interior  of 
the  eye-ball.  In  one  case  which  I  examined,  the  epithelioma 
entered  the  anterior  chamber  by  this  channel  and  was  found 
spreading  upon  the  surface  of  the  iris,  as  well  as  into  its  par- 
enchyma.    (See  Fig.  34).     Doubtlessly  the  tumor  can  also 


Fig.  34. — Epithelioma  of  the  bulbar  conjunctiva.  The  tumor  has  perforated  the  cornea, 
and  is  spreading  upon  the  surface  and  into  the  parenchyma  of  the  iris.  C.  Cornea. 
I.    Iris. 

enter  the  remaining  membranes  of  the  interior  of  the  eye  in 
such  a  manner. 


CONJUNCTIVA  BULBI  AND  EPISCLERAL   TISSUE. 


79 


Another  way  (perhaps,  a  more  frequent  one)  by  which  the 
elements  of  the  epithelioma  enter  the  interior  of  the  eye-ball, 
are  the  lymphatic  sheaths  of  the  anterior  ciliary  arteries. 
This  I  saw  in  two  cases.     (See  Fig.  35).     While  in  the  one 


Fig.  35. — Epithelioma  of  the  bulbar  conjunctiva.    An  anterior  ciliary  artery  surrounded  by 
epithelial  cells.    Nests  of  epithelial  cells  in  the  tissue  of  the  ciliary  body. 

case  the  epithelioma  had  only  entered  the  ciliary  body,  it 
had  also  invaded  the  choroid  in  the  other.  The  alterations 
produced  in  these  tissues  by  epithelioma,  resemble  those 
above  described  with  regard  to  conjunctiva,  cornea  and  scle- 
rotic. 

My  examinations  have  thus  proven,  that  epithelial  tu- 
mors of  this  region  originate  in  a  true  hyperplasia  of  the 
preexisting  epithelial  cells,  and,  furthermore,  that  the  con- 
nective-tissue, especially  the  round-cells,  undoubtedly  play 
(not  to  say  more)  an  important  and  active  part  in  their  pro- 
Stress. 


Gummata,  lupus  and  tubercles,  in  these  parts  which  have 
but  rarely  been  described,  do  not  show  any  peculiar  structure. 


8o  THE  HUMAN  EYE. 

Anglomata  of  the  conjunctiva,  do  not  seem  to  have  been 
histologically  examined  and  they  are  also  most  probably,  in 
no  way  different  from  similar  tumors  in  other  parts.  I  may' 
here  mention  that  cysticercus  and  filaria  medinensis  have 
been  observed  under  the  bulbar  conjunctiva.  | 


IV. 

IRIS. 

I.  Normal  Conditions. 

The  iris  consists  of  the  anterior  unpigmented  endothel- 
ium, the  parenchyma  and  the  posterior  pigmented  and  uveal 
layer. 

The  question  whether  the  anterior  surface  of  the  iris  is 
covered  by  a  cellular  coat,  has  up  to  a  recent  date  been  un- 
solved, Faber,  however,  has  lately  proven  that  a  continuous 
endothelial  layer  covers  the  anterior  surface  of  the  iris.  I 
have  never  been  able  to  see  this  endothelial  coat  in  hardened 
specimens,  but  only  in  fresh  ones.  I  found  the  conditions 
several  times  materially  as  stated  by  Faber. 

The  endothelial  layer  covers  the  whole  of  the  anterior  sur- 
face of  the  iris  from  the  ligamentum  pectinatum  to  the  pupil- 
lary margin.  Its  cells  are  flat,  varying  in  size,  but  mostly 
oblong  and  quadrangular  and  have  a  large  round  nucleus. 
These  cells,  however,  do  not  lie  in  one  plain  next  to  each 
other,  but  are  arranged  like  tiles,  partially,  covering  each 
other  as  J,  Arnold  has  stated  before  Faber.  The  endothel- 
ium forms,  as  it  seems,  only  a  single  layer.  Faber  states 
that  the  nuclei  of  these  cells  are  also  flattened,  and  appear 
rod-shaped  in  transverse  sections,  like  those  of  connective- 
tissue  and  organic  muscular  fibres.  These  cells  are  always 
unpigmented.  According  to  Faber  the  endothelial  layer 
ends  by  papillary  excresences  at  the  pupillary  margin. 

It  appears  that  these  endothelial  cells  are  only  loosely 
connected  with  the  underlying  tissue  or  are  very  perishable, 
which  would  explain  why  it  is  so  very  difficult  to  see  them. 

The  parenchyma  of  the  iris  appears  to  be  composed  of 
three  layers,  viz.,  a  dense  anterior,  a  loose  middle,  and  a 
dense  fibrous  posterior  layer.  They,  however,  do  not  exist  in 
reality,  as  distinctly  separate  layers,  but  they  gradually  merge 
into  each  other,  and  the  anterior  and  posterior  layers  form. 


82  THE  HUMAN  E  YE. 

— SO  to  speak — only  a  condensation  of  the  middle  one.  The 
chief  elements  of  which  the  parenchyma  of  the  iris  consists, 
are  connective-tissue  and  blood-vessels.  The  former  is  in 
different  individuals,  developed  in  a  different  degree  ;  its  cel- 
lular elements  are,  however,  always  far  more  numerous  than 
the  fibres.  The  cells  are  partially  unpigmented,  partially 
pigmented  to  a  varying  degree.  Those  of  the  anterior  and 
especially  the  posterior  layer  are  mostly  spindle-shaped  ; 
those  of  the  middle  layer  have  two  or  more  offsets,  and  fre- 
quently anastomose  with  each  other.  Moreover,  we  find, 
also  in  the  parenchyma  of  the  iris,  as  in  other  tissues,  a  num- 
ber of  wandering  cells. 

The  arteries  of  the  iris  come  from  the  circulus  iridis  major 
and  run  in  a  radiating  direction  towards  the  pupillary  margin, 
meanwhile  giving  off  numerous  smaller  branches.  Near  the 
pupillary  margin  they  form  the  circulus  iridis  minor  and  then 
a  capillary  network  between  the  fibres  of  the  sphincter  pupillae 
muscle,  or  go  directly  over  into  veins  {Faber).  The  veins  run 
again  in  a  radiating  direction  back  to  the  ciliary  bodies  and 
empty  the  blood  into  the  vorticous  veins.  According  to  y. 
ArftoM  the  blood-vessels  of  the  iris  have  an  abnormally  thick 
muscular  layer.  The  adventitia  also  is  more  developed 
than  is  commonly  the  case  in  blood-vessels  of  the  same  size. 

The  nerves  of  the  iris  which  are  hardly  less  numerous 
than  the  blood-vessels,  are  on  the  whole  arranged  like  these. 
They  come  from  the  ciliary  nerves  and  form  very  soon  after 
entering  the  iris  a  network  with  narrow  meshes  from  which 
branches  run  to  the  anterior  and  posterior  surface,  and  into 
the  sphincter  pupillae.  Nothing  certain  is  known  with  regard 
to  where  and  how  they  end.  Faber  also  describes  numerous 
ganglion-cells  in  the  iris. 

The  parenchyma  of  the  iris  contains,  moreover,  near  the 
pupillary  margin  the  sphincter  pupillae  muscle.  This  is  a 
muscular  ring  which  lies  nearer  the  posterior  than  the  ante- 
rior surface  of  the  iris.  It  consists  of  organic  muscular  fibres, 
with  a  rod-like  nucleus.  While  the  existence  of  this  muscle 
is  proven  beyond  a  doubt,  the  same  cannot  be  said  of  the 
dilatator  pupillae  described  as  its  antagonist.  The  fibres  of 
the  latter  are  said  to  run  in  a  radiating  direction,  from  the  cil- 


IRIS. 


83 


iary  margin  towards  the  sphincter  and  to  unite  with  this  mus- 
cle, after  being  bent  in  an  arch-like  way.  In  the  eyes  of  ani- 
mals, especially  of  rabbits,  these  conditions  are  plainly  to  be 
seen.  I  have,  however,  never  yet  been  able  to  distinguish  a 
dilatator  pupillae  in  the  iris  of  the  human  eye.  Iwanoff  re- 
cently tried  to  convince  us  that  the  spindle-cells  of  the  pos- 
terior layer  of  the  iris  are  muscular  fibres.  This  question  can, 
however,  hardly  be  decided  by  the  microscope  alone,  since 
we  all  know,  how  difficult  it  is  to  distinguish  by  the  mere 
form  and  shape  between  organic  muscular — and  connective- 
tissue  cells.  The  effects  of  the  different  agents  and  staining 
materials,  upon  the  tissue  give  us  more  certainty,  with  regard 
to  this  matter  and  even  in  the  finest  sections,  I  have  never  been 
able  to  see  anything  which  convinced  me  of  the  existence  of  a 
dilatator  pupillae  in  the  human  iris. 

The  posterior  surface  of  the  iris  is  covered  by  the  very 
darkly  pigmented  uveal  layer.  BrucJi  discovered  between  it 
and  the  posterior  layer  of  the  iris  a  lamina  vitrea,  like  the 
one  upon  the  choroid  and  identical  with  it,  {''  Bruc/is  mem- 
brane,"). Faber,  too  again  recently  maintained  the  existence 
of  this  membrane.  My  own  observations  force  me,  however, 
to  agree  with  those  authors  who  deny  its  existence  in  the 
human  iris. 

It  is  very  difficult  to  distinguish  the  elements  which  con- 
stitute the  uveal  layer.  With  great  care,  it  is,  however,  pos- 
sible to  recognize  a  number  of  round  or  oblong  and  irregu- 
lary  formed  cells,  which  are  densely  crowded  with  pigment- 
molecules,  so  that  we  can  scarcely  ever  see  the  round  nucleus. 
These  cells  do  not  seem  to  possess  a  cell-membrane.  Faber 
describes  still  another  kind  of  round  cell  with  a  cell-mem- 
brane. It  appears  to  me,  however,  that  the  whole  of  the 
posterior  part  of  the  uveal  layer  is  formed  by  a  continuous 
layer  of  protoplasma  in  which  pigment-molecules  are  sus- 
pended and  which  in  transverse  sections  is  often  seen  as  a 
fine  light  streak,  forming  the  posterior  margin  of  the  iris. 

This  streak  has  been  described  as  lamina  pigmenti  or 
limiting  membrane,  and  was  lately  by  i^<3;(^^r  again  considered 
to  be  a  separate  membrane.  It  is,  however,  impossible  to  de- 
tach it,  and  pathological  conditions,  of  which  we  shall  speak 


84  I^HE  HUMAN  E  YE. 

later,  do  not  allow  us  to  recognize  this  streak  as  a  separate 
limiting  membrane  of  the  iris. 

The  uveal  layer  covers  the  whole  of  the  posterior  surface 
of  the  iris  and  reaches  somewhat  farther  than  its  pupillary 
margin. 

2.  Pathological  Conditions. 

A .  Iritis  and  its  Results. 

The  different  forms  of  iritis  which  are  clinically  distin- 
guished can  not  be  so  separated  histologically.  The  large 
number  of  blood-vessels  embedded  in  the  parenchyma  of  the 
iris  must  needs  be  the  most  important  factors  in  causing  the 
symptoms  of  the  different  forms  of  iritis.  Every  inflamma- 
tion of  the  iris  is  preceded  by  hyperaemia  of  the  blood-vessels. 
Such  a  hyperaemia  of  the  iris  must  be  considered  as  a  dis- 
tinct clinical  affection  from  iritis.  Histologically  it  does, 
not  however,  appear  to  produce  pathological  alterations  in 
the  tissue  of  the  iris.  The  different  forms  of  iritis  are  chiefly 
characterized  by  the  products  of  inflammation,  the  exudates 
found  upon  the  surfaces  or  in  the  parenchyma  of  the  iris. 
We  consider  in  the  following  i.  serous  (sero-fibrinous  ;  hem- 
orrhagic), 2.  fibrinous  (plastic)  and  i.  purulent  (parenchyma- 
tous) forms  of  iritis. 

a.  Iritis  serosa  {serofibrinosa,  hemorrhagica). 

As  in  every  other  tissue,  we  find  in  the  iris,  as  soon  as  it 
is  inflamed,  a  considerable  degree  of  hyperaemia  of  the  blood- 
vessels and  an  increase  of  cells.  In  the  beginning  these  cells 
are  exclusively  emigrated,  white  blood-corpuscles,  and  no 
signs  of  proliferation  are  to  be  found  in  the  preexisting  par- 
enchymatous cells.  The  latter  begin  to  proliferate  at  a  later 
period  only.  Besides  these  new  cells,  we  find  that  the  meshes 
of  the  iris  tissue,  contain  serous  fluid,  which  makes  them 
appear  distented,  and  renders  the  whole  of  the  iris  thicker 
than  normal.  At  the  same  time  some  serous  fluid  is  exuded 
upon  the  anterior  and  posterior  surfaces  of  the  iris,  i.  e.  into 
the  posterior  and  anterior  chambers. 


IRIS. 


85 


Serous  iritis  does  not  seem  to  materially  alter  the  ante- 
rior endothelial  coat.  The  uveal  layer,  however,  is  mostly 
altered  in  such  a  way,  that  its  elements  become  remarkably 
glutinous  and  the  posterior  surface  of  the  iris  thus  becomes 
adherent  to  the  anterior  capsule  of  the  crystalline  lens.  I 
have  tried  in  vain  in  a  large  number  of  specimens  to  find  cel- 
lular elements  which  might  unite  the  iris  with  the  lens-cap- 
sule. (I  speak  here  only  of  cases  of  serous  iritis).  This  may 
explain  why  the  posterior  synechiae  caused  by  serous  iritis 
are  comparatively  easier  severed.  If  the  pupillary  edge  of 
the  iris  has  thus  become  glued  to  the  anterior  lens-capsule,  it 
often  happens  that  the  exudate  in  the  posterior  chamber, 
presses  the  periphery  of  the  iris  forward  into  the  anterior 
chamber,  and  thus  causes  the  iris  to  become,  what  has  been 
styled  "  crater-shaped."  (See  Fig.  36).  It  seems  that  this 
\ 


Fig.  36.  -Serous-iritis.  The  pupillary  edge  of  the  iris  is  adherent  to  the  anterior  lens-cap- 
sule. The  peripheral  parts  of  the  iris  are  protruding  into  the  anterior  chamber  (crater- 
shaped  iris). 

pressure  from  behind  may  produce  atrophy  of  the  blood- 
vessels and  the  parenchyma  of  the  iris,  which  conditions  were 
at  least  present  in  one  such  case  which  I  examined. 

As  stated  above,  the  endothelial  cells  upon  the  anterior 
surface  of  the  iris  do  not  seem  to  be  altered  by  serous  iritis. 
The  latter,  however,  always  produces  pathological  changes 
in  the  endothelial  cells  lying  upon  Descemefs  membrane. 
These  become  irritated  (probably  by  the  pressure  exerted 
upon  them)  and  begin  to  proliferate  partially  while  others 
become  destroyed.  In  this  way  small  deposits  are  formed 
upon  Descemefs  membrane  which  consist  of  round-cells,  free 
nuclei  and  detritus.     These  sometimes  become  detached  and 


85  THE  HUMAN  EYE. 

then  fall  to  the  bottom  of  the  anterior  chamber.  These 
changes  in  the  endothelial  cells  oi  Descemef  s  membrane,  make 
it  very  probable  that  the  endothelial  cells  upon  the  anterior 
surface  of  the  iris,  do  not  remain  unaltered,  although  I  have 
never  been  able  to  see  any  changes. 

Serous  iritis  may  perfectly  recover  and  leave  either  no  trace, 
or  only  posterior  synechiae  behind.  If  this  is  not  the  case  it 
will  become  a  chronic  iritis,  and  will  then  lead  to  a  more 
active  cell-proliferation  in  the  parenchyma  of  the  iris  which, 
ends  in  the  new-formation  of  connective-tissue,  and  the  grad- 
ual atrophy  and  destruction  of  the  preexisting  cellular  ele- 
ments. Later  on  the  blood  vessels  too,  become  atrophic, 
which  atrophy  again  produces  atrophy  of  the  whole  of  the 
iris-tissue.  This  circulus  vitiosus  is  materially  aided  in  its 
progress,  by  the  pressure  exerted  upon  the  iris-tissue  by  the 
exudation. 

A  variety  of  serous  iritis  is  the  sero-fibrinous  and  hsemor- 
rhagic  iritis.  As  far  as  I  know,  this  kind  of  iritis  has  only 
once  been  examined  histologically,  and  described  by  myself. 
Clinically  it  has  been  called  iritis  with  a  spongy  exudation. 
{Gunning,  Knapp,  Griiening). 

The  characteristic  features  of  this  kind  of  iritis  are  numer- 
ous larger  and  smaller  haemorrhages  into  the  parenchyma  of 
the  iris.  While  the  fluid  parts  of  the  blood,  are  transuded 
into  the  anterior  chamber,  its  cellular  elements  remain  lying 
in  the  parenchyma  of  the  iris,  and  there  undergo  the  well 
known  changes  of  fatty  destruction.  The  fibrine  of  the  blood 
coagulates  in  the  anterior  chamber,  and  is  later  on  gradually 
dissolved  again  from  the  cornea  backwards.  It  happens  that 
at  some  time  we  find  two  different  kinds  of  exudation  in  the 
anterior  chamber,  viz.,  a  gelatinous  part  near  the  cornea,  and 
a  sero-fibrinous  part  upon  the  iris.  (See  Fig.  37).  The  latter 
appears  under  the  microscope  as  a  network  of  very  fine 
fibrinous  threads,  not  unlike  those  found  in  the  alveoli  in 
croupous  pneumonia,  and  filled  with  serum  and  a  small  num- 
ber of  lymphatic  cells.  The  former  is  a  perfectly  uniform 
transparent  substance,  which  differs  from  the  aqueous  humor 
only  by  being  gelatinous.  The  dissolution  and  absorption 
of  this  pecuhar  exudation,  always  begins  in  the  parts  nearest 


IRIS. 


87 


the  cornea  and  progress  more  or  less  concentrically.  This 
mode  of  absorption  explains  why  at  some  time  the  exudation 
is  in  shape  and  appearance  very  much  like  an  opaque  lens, 


KiG.  37. — Hsetnorrhagic  iritis  (with  spongy  exudation).     Haemorrhages  in  the  parenchyma 
of  the  iris.    In  the  anterior  chamber  lies  a  fibrinous  and  a  gelatinous  exudation. 

which  before  it  was  duly  recognized,  led  to  frequent  errors 
with  regard  to  the  treatment  of  this  affection. 

Serous  inflammation  of  the  iris  may  spread  upon  the  cil- 
iary body  and  choroid  and  thus  produce  more  serious  symp- 
toms. It  is  also  frequently  combined  with  keratitis  leading 
to  sclerosis  of  the  involved  part  of  the  cornea. 

b.  Iritis  fibrinosa  {plasticd). 

Fibrinous  iritis  shows  besides  hyperaemia  of  the  blood- 
vessels and  an  increase  of  cellular  elements  in  the  parenchyma 
of  the  iris,  a  fibrinous  exudation.  This  exudation  generally 
appears  first  at  the  pupillary  edge  and  we  then  find  besides 
the  adhesion  between  the  posterior  surface  of  the  iris,  and 
the  anterior  lens-capsule  (which  we  also  found  in  cases  of 
serous  iritis),  an  amorphous  fibrinous  coagulum  upon  the 
pupillary  region  of  the  anterior  lens-capsule.  The  exudation 
is  but  seldom  found  upon  the  posterior,  and  yet  more  rarely 
upon  the  anterior  surface  of  the  iris  in  the  earlier  periods  of 
the  disease.     The  fibrinous  coagulum  usually  contains  some 


88 


THE  HUMAN  EYE. 


round-cells.  If  the  process  be  arrested  at  this  period  the 
fibrine  may  be  dissolved,  and  totally  absorbed.  It  is,  however 
very  frequently  found  that  the  disease  progresses  and  the 
fibrine  becomes  an  organized  tissue.  More  round  cells  wan- 
der into  it  and  assume  the  spindle-shape,  while  the  fibrine 
is  destroyed.  We  then  find  at  some  later  period  instead  of 
the  fibrinous  coagulum,  a  delicate  membrane  consisting  of 
spindle-cells,  which  however,  later  on  is  changed  into  a 
fibrous  and  tough  connective-tissue.  This  membrane,  gener- 
ally called  pupillary  membrane,  usually  spreads  a  short 
distance  upon  the  anterior  and  posterior  surface  of  the  iris. 
(See  Fig.  38).     At  a  later  period  we  frequently  find  that  the 


Fig.  38.— Plastic  iritis.    Pupillary  membrane. 

blood-vessels  of  the  iris  have  grown  into  the  pupillary  mem- 
brane. When  this  new-formed  connective-tissue  shrinks, 
it,  of  course  drags  upon  the  iris,  which  thus  is  drawn  towards 
one  side  or  towards  the  centre  of  the  pupil  and  becomes 
atrophic.  If  at  the  same  time  some  fibrine  has  been  exuded 
upon  the  posterior  surface  of  the  iris,  this  may  also  be  trans- 
formed into  connective-tsssue,  which  later  on  produces  an 
adhesion  between  iris  and  lens-capsule,  materially  different 
from  the  common  pupillary  adhesion. 

As  above  stated,  fibrinous  exudation,  is  but  seldom  de- 
posited upon  the  anterior  surface  of  the  iris.  It  seems  to 
me  that  this  happens  only  when  the  changes  in  the  pupillary 
region  have  taken  place,  and  the  posterior  surface  of  the  iris 
has  become  adherent  to  the  lens.    In  rare  cases  this  fibrinous 


IRIS. 


89 


exudation  is  deposited  in  such  a  quantity,  upon  the  anterior 
surface  of  the  iris  that  the  anterior  chamber  is  perfectly  filled 
with  it.  The  exudation  may  here  also  become  organized 
and  vascularized.  Membranes  thus  formed,  generally  have  a 
lamellar  structure,  similar  to  the  corneal  tissue.  They  fre- 
quently contain  old  or  recent  haemorrhages.     (See  Fig.  39). 


Fig.  39.  Plastic  iritis.— New-formed  connective-tissue  upon  the  anterior  surface  of  the  iris. 
This  tissue  is  lamellar  and  contains  blood-vessels.     H.  A  large  haemorrhage. 

The  alterations,  caused  by  the  above  described  conditions 
in  the  parenchyma  of  the  iris,  produce  perfect  atrophy  of 
this  membrane.  The  uveal  layer  frequently  shows  a  very 
peculiar  appearance.  In  the  beginning  of  the  affection,  it  is 
very  much  thickened,  and  when  the  fibrinous  exudation  lying 
upon  it  becomes  organized,  it  seems  that  the  protoplasma,  in 
which  the  pigment-molecules  are  suspended  is  consumed. 
The  pigment  molecules,  thus  freed,  are  drawn  into  the  new- 
formed  connective-tissue,  and  the  uveal  layer  appears  several 
times  thicker  than  it  does  in  the  normal  condition. 

Fibrinous  inflammation  may,  of  course,  also  spread  from 
the  iris  upon  the  ciliary  body  and  choroid.  Furthermore,  the 
communication  between  the  vitreous  body  and  the  anterior 
chamber  being  perfectly  cut  off,  the  intra-ocular  pressure,  may 
become  increased  and  lead  to  results  to  be  detailed  farther  on. 

c.  Iritis  purutertta  {parenchymatosd). 

While  in  iritis  serosa  and  fibrinosa  we  found  the  exuda- 
tion to  contain  but  few  cells,  the  latter  are  the  prevalent  part 
of  the  exudation  of  a  purulent  iritis. 

Hyperaemia  of  the  blood-vessels  is  at  once  followed  by  a 
considerable  emigration  of  round-cells,  and  proliferation  of 


90 


THE  HUMAN  E  YE. 


the  parenchymatous  cells  of  the  iris.  This  causes  the  iris 
to  become  rapidly  swollen,  and  pus-cells  wander  into  the 
anterior  chamber,  at  first  probably  through  the  meshes,  of 
the  ligamentum  pectinatum.  If  the  changes  progress,  we 
find  that  all  the  elements  forming  the  tissue  of  the  iris  are 
gradually  destroyed.  The  proliferating  parenchymatous  cells 
lose  their  pigment-molecules,  which  then  are  lying  free  be- 
tween the  cells,  and  free  nuclei.  Later  on,  the  endothelial 
cells,  the  muscular  fibres,  and  lastly  the  blood-vessels  take  an 
active  part  in  the  new-formation  of  round-cells.  We  find 
these  conditions,  however,  well  pronounced  only  in  cases  of 
purulent  panophthalmitis,  and  we  may  then  see  the  iris 
replaced  by  a  mass  of  round-cells  and  free  nuclei,  filling  the 
anterior  chamber  without  showing  any  traces  of  muscles, 
blood-vessels  or  even  pigment,  and  in  no  way  reminding  one 
of  the  normal  conditions  of  the  iris.  We  spoke  of  a  similar 
affection  observed  in  the  cornea,  and  called  keratomalacia ; 
it  might  be  very  appropriate  to  call  this  condition  of  the  iris 
iridomalacia.     (See  Fig.  40). 


Fig.  40. — Purulent  iritis. 

Parenchymatous  iritis  may  also  appear  as  a  merely  local 
affection,  in  the  shape  of  a  gumma  or  tubercle.  In  both 
cases  we  find  local  swelling  and  accumulation  of  round-cells. 
Colberg  described  a  case  of  gumma  of  the  iris.  He  found 
free  nuclei,  gummy  intercellular  substance  and  new-formed 
connective-tissue.  These  cell  accumulations  gradually  under- 
go a  fatty  metamorphosis,  and  the  detritus  is  usually  emptied 
into  the  anterior  chamber,  after  the  anterior  surface  of  the  iris 
has  been  ruptured.  A  small  scar  is  generally  the  only, 
remaining  trace  of  such  a  local  parenchymatous  iritis.  Gumma 
as  well  as  tubercle  may,  however,  grow  so  large  as  to  touch 


IRIS. 


91 


the  posterior  surface  of  the  cornea.  Anterior  synechia  may- 
be thus  formed  with  or  without  perforation  of  the  cornea. 
This  is  probably  the  only  way  in  which  anterior  synechias  of 
the  iris,  is  formed  without  preceding  perforation  of  the  cornea. 
Diffuse  purulent  iritis,  as  stated  above  is  chiefly  found  in 
cases  of  purulent  panophthalmitis.  It  may,  however,  also  be 
the  primary  affection,  and  lead  to  purulent  panophthalmitis. 

The  Results  of  Iritis. 

If  iritis  does  not  heal  at  an  early  stage,  or  if  the  in- 
flammation, does  not  lead  to  the  perfect  destruction  of  the 
eye-ball,  by  spreading  over  the  remaining  parts  of  this  organ, 
it  leaves  changes  behind  which  always  enable  us  to  make  a 
a  sure  diagnosis,  with  the  aid  of  the  microscope. 

a.  Syne  chics  of  the  Iris. 

The  most  frequent  results  of  iritis  are  synechias  of  the 
iris,  especially  posterior  ones,  anterior  ones  being  only  in  ex- 
ceptional cases  caused  by  iritis.  The  name  synechias  is  here 
applied  to  the  adhesion  between  the  iris,  (especially  of  its 
pupillary  edge),  and  the  anterior  capsule  of  the  lens. 
Synechias  are  caused  by  all  the  three  forms  of  iritis.  In 
cases  of  simple  synechias,  I  never  could,  find  an  organized 
tissue,  between  iris  and  lens-capsule.  In  transverse  sections 
the  uveal  layer  simply  lies  close  upon  the  lens-capsule.  If 
we  try  to  sever  the  synechias,  the  uveal  layer,  is  torn  and 
remains  partly  upon  the  lens-capsule,  partly  in  connection 
with  the  iris.  I  suppose  chemical  processes  cause  these  ad- 
hesions which  the  microscope  cannot  possibly  detect.  The 
conditions  are  very  different  when  the  whole  of  the  posterior 
surface  of  the  iris  is  glued  to  the  lens,  in  the  pupillary  mem- 
branes and  the  new-formed  tissue  upon  the  anterior  surface 
of  the  iris.  Here  we  always  find  anew-formed  connective- 
tissue,  which  at  first  contains  a  large  number  of  cells,  and 
later  on  becomes  tougher,  denser,  and  loses  the  cellular  ele- 
ments. It  is  then  generally  vascularized  by  new-formed 
blood-vessels  starting  from  the  blood-vessels  of  the  iris. 
(See   Fig.  41.)     During  the  period   of  retraction,  this  new- 


92 


THE  HUMAN  E  YE. 


formed  tissue  drags  upon  the  tissue  of  the  iris  and  causes 
it  to  atrophy. 


Fi;..  41. — New-formed  connective-tissue  uniting  tiie  posterior  surface  of  the  iris  with  the 
anterior  lens-capsule  after  plastic  iritis. 

b.  Atrophy  of  the  Iris. 

Besides  the  just  mentioned  atrophy  of  the  iris,  caused  by 
pressure  and  tearing  from  parts  outside  the  parenchyma  of 
the  iris,  atrophy  of  the  latter  may  be,  and  is  frequently  the 
result  of  chronic  iritis.  The  atrophy  is  then  the  direct  con- 
sequence of  the  new-formation  of  connective-tissue,  in  the 
parenchyma  of  the  iris,  or  the  pressure  exerted  upon  it  by  the 
exudation  of  serum  into  its  meshes  and  interstices.  It  seems 
that  the  first  to  suffer  from  atrophy,  are  the  pigmented 
parenchyma  cells.  They  undergo  fatty  degeneration,  become 
granular,  and  are  broken  up.  Their  pigment  is  then  found 
scattered  about  in  the  tissue  ;  later  on  it  may  nearly  alto- 
gether disappear.  The  last  to  become  atrophic  are  the  uveal 
layer  and  the  muscular  tissue  of  the  sphincter  pupillae,  and 
even  in  the  highest  degrees,  of  atrophy  of  the  iris,  they  are 
not  totally  destroyed. 

In  one  case  of  very  far  advanced  atrophy  of  the  iris,  I 
found  the  anterior  endothelium,  in  a  state  of  colloid  meta- 
morphosis. (See  Fig.  42.)  With  a  low  magnifying  power  it 
appeared  like  a  new-formed  transparent  lamella,  covering  the 
anterior  surface  of  the  iris.  (Similar  vitreous  lamellae,  upon  the 
iris  have  been  described  by  a  number  of  authors,  and  declared 
to  be  inflammatory  new-formations  ;  perhaps,  they  ought  to 


IRIS. 


93 


have  been  explained  in  the  same  way  as  the  one  under  con- 
sideration). With  a  high  power  it  was  easily  seen  to  consist 
of  endothelial  cells,  filled  with  colloid  substance. 


Fig:.  42— Iritis  chronica.    Atrophy  of  the  iritis  and  colloid  metamorphosis  of  its  anterior 

endothelial  coat. 

Atrophy  of  the  whole  iris,  of  course,  invoh'es  also  its 
blood-vessels  and  nerves. 

B.  Injuries  to  the  Iris  and  their  Results, 
Injuries  to  the  iris  are  mostly  combined  with  an  injury  to 
the  cornea  or  sclerotic  or  even  more  parts  of  the  eye-ball.  It 
is  easily  understood  that  the  histological  conditions  are 
accordingly  complicated.  We  will  however,  here  mention 
only  those  injuries  which  involve  cornea,  or  sclerotic  and  iris, 
and  those  which  concern  the  iris  alone. 

Foreign  bodies  which  enter  the  eye,  only  very  seldom 
remain  lodged  in  the  tissue  of  the  iris.  They  either  perforate 
it  and  pass  farther  on,  or  rebound  and  fall  into  the  anterior 
chamber.  If  however,  they  remain  lodged  in  the  iris,  they 
produce  at  first  a  local,  later  on  a  diffuse  iritis,  which  gener- 
ally assumes  a  purulent  character.  More  does  not  seem  to 
be  known,  with  regard  to  the  anatomical  conditions.  Foreign 
bodies  intentionally  brought  into  the  iris  of  animals,  lead  also 
to  the  growth  of  sarcomatous  new-formations. 

The  injury  may  sever  the  tissue  of  the  iris  to  a  varying 
extent.  The  wound  may  lie  at  the  pupillary  edge,  or  in  the 
part  between  it  and  the  ciliary  margin,  or  at  the  latter,  or  the 
whole  of  the  breadth  of  the  iris,  may  be  rent  apart  in  a 
radiary  direction,  or  it  may  reach  from  the  sphincter  or  ciliary 
edge,  into  the  part  between  the  two.  If  the  iris  tissue  is  thus 
once  severed,  the  gap  generally  remains  a  permanent  one. 


94 


THE  HUMAN  E  YE. 


The  edges  of  such  a  wound  heal  through  a  small  amount  of 
fibrine  which  becomes  exuded  and  organized  upon  them. 
The  healing  process  after  wounds  caused  by  operations  too, 
show  nothing  peculiar. 

Rents  of  the  sphincter  edge  of  the  iris  (coloboma)  and  the 
separation  of  the  ciliary  edge  of  the  iris  from  the  ligamentum 
■  pectinatum  and  the  ciliary  body  (iridodialysis)  are  not  unfre- 
quently  caused  by  injuries  which  do  not  at  the  same  time 
rupture  either  of  the  hard  membranes  of  the  eye-ball.  Rup- 
tures of  the  part  of  the  iris,  between  its  pupillary  and  ciliary 
margins,  are  probably  always  combined  with  wounds  of  one 
or  both  of  the  hard  membranes. 

If  the  cornea  or  the  corneo-scleral  margin  has  been  rup- 
tured by  the  injury,  the  aqueous  humor  will  flow  out,  and 
the  either  wounded  or  normal  iris,  becomes  entangled  in  the 
wound-lips,  or  is  thrown  further  into  the  wound-canal.  This 
causes  the  formation  of  an  anterior  synechia  (leucoma  ad- 
haerens)  or  a  prolapse  of  the  iris,  which  may  either  become 
reduced  or  remain  stationary.  If  the  prolapse  of  the  iris 
remain  stationary,  the  prolapsed  part  may  either  decay,  and 
fall  off  (and  thus  again  an  anterior  synechiae  be  the  result)  or 
it  may  become  the  starting  point  of  a  granuloma  of  the  iris, 
of  which  more  later  on. 

The  histological  conditions  in  cases  of  anterior  synechiae, 
of  the  iris  have  been  spoken  of  above  (See  chapter  I).  I 
must  mention  here,  however,  a  condition  resulting  from 
anterior  synechiae,  and  involving  the  iris  only.  I  mean  the 
formation  of  serious  cysts  of  the  iris.  Von  Wecker  &  Knapp 
have  stated  (and  I  once  had  occasion  to  confirm  their 
statement)  that  serous  cysts  of  the  iris  may  be  formed,  if 
a  fold  of  this  membrane,  becomes  adherent  to  the  posterior 
surface  of  the  cornea  (or  to  a  wound-canal  in  the  latter),  that 
is,  that  the  parenchyma  of  the  iris  takes  no  active  part  in  the 
formation  of  these  cysts.  The  walls  of  such  a  serous  cyst  of 
the  iris  which  I  had  occasion  to  examine  were  two-thirds 
formed  by  the  atrophic  iris,  and  one-third  by  the  posterior 
surface  of  the  cornea,  and  were  thus  perfectly  lined  with  the 
endothelium  of  the  anterior  chamber.     (See  Fig.  43.) 

The  cavity  formed  in  such  a  way  inside  the  anterior  cham- 


IRIS. 


95 


ber,  becomes   larger  through  the   pressure  of  the  aqueous 
humor  secreted  by  it.      Von  Wecker  states  that  such  a  cyst 


Fig.  43 — So-called  cyst  of  the  iris,  formed  after  an  injury  to  the  cornea.  The  walls  of  the 
cyst  are  formed  by  Descemet's  membrane,  the  atrophic  iris  and  some  new-formed  con- 
nective-tissue, and  lined  with  the  endothelium  of  the  anterior  chamber. 

may  separate  itself  at  a  later  period  from  the  cornea.  This 
appears  rather  improbable  from  the  anatomical  conditions, 
and,  moreover,  clinical  experience  shows  that  these  cysts 
are  firmly  adherent  to  the  cornea,  and  therefore  are  nearly 
always  ruptured  in  the  attempt  to  remove  them  by  an  opera- 
ration. 

What  we  described  above  as  crater-shaped  iris,  that  is, 
the  bulging  and  atrophy  of  the  periphery  of  this  membrane, 
subsequent  to  circular  posterior  synechia  of  the  pupillary 
margin,  is  by  von  Wecker  enumerated  among  the  cysts  of 
the  iris. 

Some  authors  described  another  variety  of  cyst,  in  the 
parenchyma  of  the  iris  filled  with  atheromatous  substance, 
and  always  resulting  from  an  injury  which  has  been  called 
"  epidermoidoma."  Krause's  observations  leave  no  doubt 
that  these  cysts  are  caused  by  epithelial  cells,  from  the  hair- 
follicles  of  the  eye-lashes,  which  are  thrown  into  the  pa- 
renchyma of  the  iris  during  the  infliction  of  an  injury,  arc 
there  retained,  and  then  begin  to  proliferate.  This  is  the 
more  probable,  as  generally  in  these  cases  one  or  more  ciliie 
were  found  in  the  anterior  chamber  or  in  the  tissue  of  the 
iris. 

It  follows  therefore  from  the  facts  above  stated,  that 
serous  cysts  of  the  iris  are  improperly  so-called,  and  originate 


96 


THE  HUMAN  E  YE. 


in  an  injury  followed  by  the  adhesion  of  a  fold  of  the  iris  to 
the  cornea.  Atheromatous  cysts  lie  really  in  the  parenchyma 
of  the  iris,  and  are  usually  caused  by  an  injury  without  the 
formation  of  anterior  synechise  between  this  membrane  and 
the  cornea. 

The  conditions  resulting  from  prolapse  of  the  iris,  were 
studied  by  me  some  time  ago,  experimentally  on  the  eyes  of 
animals.  The  results  of  these  examinations  were  published, 
without  however,  applying  the  lessons  they  taught  uncon- 
ditionally to  the  human  eye.  Numerous  specimens  from  the 
human  eye  have  since  then,  taught  me,  that  I  would  have 
been  justified  in  doing  so. 

Very  soon  after  the  iris  has  prolapsed  into  a  wound-canal 
of  the  cornea  or  sclerotic,  it  becomes  infiltrated  with  blood 
in  consequence  of  the  stasis  of  its  blood-vessels.  If  the  pro- 
lapse protrudes  through  the  cornea,  it  may  become  necrotic 
and  be  thrown  off.  The  outer  orifice  of  the  wound-canal  is 
then  covered  by  new-formed  connective-tissue  and  epithelium, 
and  we  thus  find  again  the  conditions  of  an  anterior  synechia. 
If  the  prolapse  is  small,  it  may  be  covered  in  toto  with  scar- 
tissue  (See  Fig.  44),  into  which  a  fibrinous  exudation  coming 


Fig.  ^4.~  Incarcerated  iris.    Small  prolapse  of  the  iris  into  a  corneal  wound,  covered  with 
new-formed  connective-tissue  and  epithelium. 

from  the  iris  is  gradually  transformed.     This  is  especially  the 


IRIS. 


97 


case  when  the  iris  has  prolapsed  at  the  corneo-scleral  margin 
(for  instance  after  operations  in  that  region).  The  epithe- 
lium which  finally  covers  such  a  prolapse  in  the  corneo-scleral 
region,  takes  the  greater  part  of  its  origin  from  the  conjunc- 
tiva. The  final  stationary  condition  has  received  the  name 
of"  incarceration  "  of  the  iris. 

Injuries  to  the  eye  without  inflicting  wounds  may  some- 
times cause  a  part,  or  the  whole  of  the  pupillary  edge  of  the 
iris  to  be  tilted  backwards.  Such  cases  have,  however,  it 
seems,  never  been  microscopically  examined. 

• 
C.  Tumors  of  the  Iris. 

a.  Granuloma  Traumaticum. 

Although  clinicists  have  described  a  genuine  (non-tran- 
matic)  granuloma  of  the  iris,  only  the  traumatic  one  has  so 
far  been  microscopically  studied.  The  results  of  my  own 
examinations  of  three  such  cases,  perfectly  agree  with  those 
of  Hirschberg  and  Steinheim. 

Prolapse  of  iris,  or  those  parts  which  are  exposed  to  the 
air  through  the  destruction  of  the  cornea,  often  become  the 
origin  of  such  tumors.  The  latter  consist  of  round  and  small 
spindle-cells,  between  which  are  found  a  small  amount  of 
connective-tissue  and  new-formed  blood-vessels.  (See  Fig. 
45).  The  tumor  may  or  may  not  be  covered  by  epithelium. 
It  is  probable  that,  like  other  granulomata  this,  also  may  be 
transformed  into  connective-tissue  and  thus  heal  by  itself. 

HirscJiberg  and  Von  Weckcr  also  count  among  the  granulo- 
mata of  the  iris  a  vascular  tumor,  described  by  Mooren,  but 
not  examined  anatomically.  Schirmer  mentioned  a  "  cav- 
ernous "  tumor  of  the  iris  which  probably  belonged  to  the 
same  class. 

b.  Melanoma. 

Knapp  was,  as  far  as  I  know,  the  first  to  describe  sim- 
ple melanoma  of  the  iris  after  having  seen  a  specimen  of 
J.  Arnold's.  It  "  consisted  of  circumscribed  accumulations  of 
stroma-cells  of  the  iris,  the  larger  part  of  which  were  pig- 
mented, had  many  offsets  and  anastomosed  with  each  other. 


98 


THE  HUMAN  EYE. 


They  passed  without  a  sharp  boundary  into  the  neighboring 
tissue,  and  the  remainder  of  the  iris  was  normal."    This  kind 

Gr 


Fig.  45. — Traumatic  granuloma  of  the  iris  after  this  membrane  has  prolapsed.  Gr.  Gran- 
uloma. C.  Cornea.  D.  Descemet's  membrane.  Ir.  Iris.  Cc.  Ciliary  body.  L.C 
Lens-capsule. 

of  tumor  is  certainly  very  rare.  Like  all  the  so-called  benign 
melanomata,  it  is  said  to  be  able  at  any  time  to  assume  a 
malignant  character. 

c.  Leucosarcoma  and  Melanosarcoma. 

Primary  sarcomata  of  the  iris  are  very  rarely  met  with. 
Only  four  such  cases  have  so  far  been  anatomically  examined 
and  described  {Dreschfeld,  Knapp,  Hirschberg,  Kipp.) 

It  seems  that  the  new-formation  takes  its  origin  from  the 
parenchyma  of  the  iris.  In  Dreschfeld' s  case  only,  it  was 
said  to  have  started  from  the  connective-tissue  between  the 
muscular  fibres. 

From  these  different  descriptions,  we  know  of  unpig- 
mented  {Kipp)  pigmented  {Hirschberg)  spindle-cell  sarcoma, 
and  pigmented  round-cell  sarcoma.  All  of  the  tumors  were 
very  vascular.  Judging  from  the  structure  of  the  iris,  we 
may  expect  (and  the  descriptions  prove  it),  that  the  pig- 
mented tumors  have  also  some  unpigmented  parts  and  vice 
versa.  Dreschfeld  found  some  small  nests  of  organic  muscu- 
lar fibres  in  his  case,  and  considered  this  proof,  that  the 
tumor  originated  in  the  intra-muscular  connective-tissue. 

Sarcoma  of  the  iris  seems  to  grow  comparatively  slowly. 


CORPUS  CI  LI  A  RE.  gg 

It  causes,  like  other  intra-ocular  tumors,  glaucoma,  and  leads 
to  destruction  of  the  eye. 

Metastic  tumors  caused  by  primary  sarcoma  of  the  iris, 
have  been  clinically  observed. 

V.  Corpus  Ciliare. 
I.  Normal  Conditions. 

The  tissue  of  the  ciliary  body  consists  of  the  same  ele- 
ments as  that  of  the  iris.  We  find  here  as  the  outermost  layer 
(near  the  sclerotic)  an  endothelial  coat,  then  the  parenchyma 
and  inwards  from  this,  the  pigmented  uveal  layer  which, 
moreover,  is  here  covered  by  another  layer,  viz.,  the  ciliary 
part  of  the  retina.  While  the  surfaces  of  the  iris  are  com- 
paratively smooth,  the  inner  surface  of  the  ciliary  body,  has  a 
large  number  of  processes  and  corresponding  indentations. 
The  former  are  called  the  ciliary  processes. 

The  parenchyma  of  the  ciliary  body,  like  that  of  the  iris, 
consists  in  the  main  part  of  cellular  elements.  We  here 
again  find  round  unpigmented  cells,  and  cells  with  offsets 
which  are  either  pigmented  or  unpigmented.  The  pigmented 
cells  with  offsets  are  very  numerous,  only  in  the  eyes  of 
negroes.  In  the  eyes  of  the  white  races,  the  tissue  of  the 
ciliary  body  has  chiefly  unpigmented  cells.  Besides  the  cells, 
we  find  a  larger  quantity  of  connective-tissue  fibres,  and  elastic 
fibres  in  the  ciliary  body,  than  in  the  iris.  The  connective- 
tissue  prevails  in  the  outer  parts  (near  the  sclerotic),  while  the 
cellular  elements  form  mainly  the  inner  layers  of  the  ciliary 
body. 

Embedded  in  this  tissue  is  the  ciliary  muscle.  It  con- 
sists, as  well  known,  of  circular  (equatorial)  and  longitudinal 
(meridional)  fibres.  The  longitudinal  fibres  lie  in  the  outer, 
the  circular  ones  more  in  the  inner  part,  of  the  ciliar}''  body. 
The  two  kinds  of  fibres  are,  however,  not  perfectly  dis- 
tinct from  each  other,  as  a  fibre  may  at  first  run  in  a  longi- 
tudinal and  then  in  a  circular  direction  and  vice  versa.  The 
elements  of  this  muscle  are  organic  muscular  fibres. 

Iwanoff  was  the  first  to  point  out  that  the  proportion, 
between  the  two  kinds  of  fibres  (circular  and  longitudinal), 


lOO  THE  HUMAN  E  YE. 

varies  in  different  eyes.  He  found  that  in  myopic  eyes,  that 
is,  eyes  which  are  very  long,  the  longitudinal  fibres  prevail 
(See  Fig.  46),  while  in  hypermetropic,  that  is,  short  eyes,  the 


Fig.  46. — Ciliary  body  from  a  myopic  eye. 

circular  fibres,  which  are  but  few  in  an   emmetropic  eye,  are 
very  numerous.     (See  Fig.  47).     Rvanoff,  however,   has   at 


Fig.  47. — Ciliary  body  from  an  hypermetropic  eye. 

the  same  time  to  confess  there  are  many  exceptions  to  these 
conditions. 

To  explain  the  mode  in  which  accommodation  takes 
place,  a  number  of  hypotheses  have  been  put  forward  and, 
strange  to  say,  most  of  them  would  presume  just  the  reverse 
condition,  of  the  ciliary  muscle  from  that  which  we  frequently 
find.  This  has  already  been  pointed  out  by  Loring.  It  is 
not  the  place  here  to  speak  of  the  physiological  action  of  this 
muscle,  but  I  have  to  state,  that  in  eyes  suffering  from  ciliary 


CORPUS  CI  LI  A  RE.  lOI 

or  total  staphyloma  we  find  the  same  conditions,  with  regard 
to  the  ciliary  muscle  as  in  myopic  eyes,  i.  e.  only  longitudinal 
fibres.  This  would  show  that  any  stretching  of  the  ciliary 
muscle,  is  enough  to  produce  such  conditions. 

The  question,  how  the  ciliary  muscle  acts,  when  the  eye 
accommodates,  can  only  be  satisfactorily  solved,  by  closely 
studying  the  development  of  this  muscle,  and  it  would,  be 
very  important  to  know,  for  instance,  whether  in  a  case  of 
non-progressive  myopia  this  muscle  presents  the  same  ar- 
rangement soon  after  birth,  that  it  does  in  the  later  periods  of 
progressive  myopia.  The  authors  on  the  development  of 
the  eye  have,  it  seems,  all  neglected  to  study  this  point, 
which  is  of  such  great  importance.  In  the  eyes  of  two  newly 
born  children  I  only  found  longitudinal  fibres,  although  the 
shape  of  the  eyes  impressed  me  as  being  that  of  emmetropic 
ones. 

The  fibres  of  the  ciliary  muscle  are  joined  anteriorly  in  a 
tendon  which  passes  over  into  Descemefs  membrane,  and  the 
posterior  lamellae  of  the  cornea  in  the  way,  described  above 
(See  Chapter  I).  Posteriorly  the  muscular  fibres  end  in  the 
outer  layers  of  the  choroid  in  peculiar  star-like  formations 
{leropheeff,  Iwanoff),  some  of  them  pass  into  the  sclerotic. 

On  equatorial  sections  through  the  ciliary  body,  it  is  seen 
that  the  separation  into  longitudinal  and  circular  fibres,  which 
is  so  well  pronounced  in  meridional  sections,  is  only  apparent, 
and  that  the  fibres  interlace  at  all  sorts  of  angles. 

The  blood-vessels  of  the  ciliary  body  come  from  the 
arteriae  ciliares  posteriores  longae  and  the  arterias  ciliares  an- 
teriores.  Their  structure  shows  nothing  peculiar.  The 
larger  part  of  their  branches  lie  in  the  layers  to  the  inner  side 
of  the  ciliary  muscle.  The  veins  of  the  ciliary  body  conduct 
the  blood  either  to  the  small  veins  coming  from  the  cornea 
(resp.  conjunctiva),  or  to  the  vorticous  veins  {Leber). 

The  nerves  constituting  a  net- work  of  the  ciliary  body, 
come  from  the  ciliary  nerves.  They  lie  chiefly  upon  the 
outer  surface  of  the  ciliary  muscle,  from  where  smaller 
branches  enter  the  latter.  It  is  not  known  how  and  where 
they  end. 

If  we  sever  the  ciliary  body  (or  choroid)  from  the  sclero- 


102  THE  HUMAN  E  YE. 

tic,  a  number  of  fibres  will  remain  in  connection  with  the 
latter,  which  have  been  called  the  lamina  fusca.  This 
lamina  is,  however,  not  an  independent  membrane.  As 
stated  above,  some  of  the  fibres  of  the  ciliary  muscles  insert 
themselves  into  the  sclerotic,  moreover,  connective-tissue 
fibres  from  the  sclerotic  enter  the  ciliary  body,  (and  choroid) 
and  vice  versa.  It  is  therefore  easily  comprehended  that  in 
separating  the  two  layers,  we  tear  these  fibres  apart.  The  part 
remaining  adherent  to  the  sclerotic  is  the  lamina  fusca,  the 
part  remaining  connected  with  the  ciliary  body  (or  choroid)  is 
the  so-called  lamina  suprachorioidea.  Both  of  these  parts  are 
formed  by  the  fibres  joining  the  hard  membranes  of  the  eye 
and  the  uveal  tract  which  {J.  Arnold^  have  one  and  the  same 
origin  in  the  embryo.  A  structureless,  homogeneous  inter- 
fibrillar  substance,  as  described  by  Iwanoff,  I  cannot  find. 
The  meshes  between  the  fibres  contain,  however,  a  serous 
(lymphatic)  fluid  which  coagulates  when  the  eye  is  hardened. 

Between  these  fibres  lie  a  large  number  of  pigmented 
cells.  These  are  very  irregular  in  shape,  and  have  mostly 
short,  broad  offsets,  and  are  flat.  Their  large  oval  or  round 
nucleus  is  unpigmented.  Besides  these  pigmented  cells  of 
various  shapes,  {Iwanoff  also  described  round  ones),  there 
are  unpigmented  endothelial  and  lymph-cells.  The  latter 
hafrve  nothing  peculiar.  The  existence  of  the  former  is  proven 
by  staining  with  nitrate  of  silver.  They  form  a  continuous 
coat  upon  the  inner  surface  of  the  sclerotic,  and  the  outer 
surface  of  the  ciliary  body  (and  choroid),  perforated  only  by 
the  fibres  running  from  one  of  these  parts  to  the  other 
Endothelial  cells  also  lie  upon  the  latter  in  the  same  way  in 
which  we  found  them,  adherent  to  the  fibres  of  the  ligamen- 
tum  pectinatum. 

The  parenchyma  of  the  ciliary  body  is,  on  its  inner  sur- 
face, covered  by  a  thin,  elastic  vitreous  membrane  which  is, 
however,  only  continuous  upon  the  so-called /^ri-  non-plicata 
Anteriorly  to  this  it  is  perforated,  and  thus  forms  a  net-work, 
the  meshes  of  which  are  oblong  in  a  longitudinal  direction 
{Iwanoff).  I  can  not,  however,  perfectly  agree  with  Iwanoff, 
who  could  trace  this  vitreous  membrane  even  upon  the  ciliary 
processes,  for  I  never  found  it  there. 


CORPUS  CI  LI  A  RE. 


103 


The  uveal  layer  of  the  ciliary  body,  lies  on  the  inner  sur- 
face of  this  vitreous  membrane.  It  consists  of  cells  which 
vary  considerably  in  shape  and  size.  They  are  densely  filled 
with  pigment-molecules,  which  leave  only  the  round  nucleus 
free.  The  cells  are  united  to  each  other  by  a  structureless 
cementing  substance  and  form  one,  or  sometimes  several 
layers.  It  is  very  difficult  to  distinguish  the  single  cells 
upon  the  ciliary  processes  and  the  uveal  layer  here  greatly 
resembles  that  of  the  iris.  Where  the  lamina  vitrea  forms 
the  above  described  network,  the  pigmented  cells  lie  in  the 
meshes. 

Upon  the  inner  surface  of  the  uveal  layer  of  the  ciliary 
body,  lies  the  pars  ciliaris  retinae.  The  elements  of  this  mem- 
brane are  according  to  the  latest  authors,  to  be  considered  as 
the  continuation  of  Mueller  s  supporting  fibres  of  the  retina. 

The  ciliary  part  of  the  retina,  consists  of  one  layer  of  more 
or  less  cylindrical  cells,  which  gradually  decrease  in  size 
towards  the  insertion  of  the  iris.  They  are  unpigmented  and 
have  a  round  or  oval  nucleus  which  lies  near  their  basis. 
Where  the  vitreous  body  lies  upon  them,  they  are  flat  or 
cone-shaped,  and  some  of  them  have  small  offsets.  We  find 
sometimes  a  very  thin  vitreous  membrane  lying  upon  them, 
which  is  probably  the  remainder  of  the  membrana  limitans 
interna  of  the  retina. 

2.  Pathological  Conditions. 

A.  Cyclitis  and  its  Results. 

From  the  similarity  which  exists  between  the  structure 
of  the  iris  and  the  ciliary  body,  and  their  direct  connection,  we 
may  a  priori  expect  to  find  the  pathological  processes  of  the 
ciliary  body  analogous  to  those  of  the  iris. 

The  three  forms  of  cyclitis  which  will  be  spoken  of  pres- 
ently, and  which  mostly  are  found  at  the  same  time  with 
similar  affections  in  the  iris  or  choroid,  are:  i.  serous  (sero- 
fibrinous), 2.  fibrinous  (plastic)  and  3.  purulent  cyclitis. 

a.  Cyclitis  Serosa. 
Serous  cyclitis  is  hardly  ever  found  without  coexisting 


I04 


THE  HUMAN  EYE. 


serous  iritis.  The  ciliary  body  in  this  disease  appears  very 
hyperaemic,  and  the  tissue  around  the  blood-vessels  contain  a 
few  emigrated  white  blood-corpuscles.  The  exudation  char- 
acteristic of  this  kind  of  cyclitis  is  found  in  the  posterior 
chamber  and  the  vitreous  body,  sometimes  also  in  the  tissue 
of  the  ciliary  body  itself.  If  the  pupillary  margin  of  the  iris 
is  at  the  same  time  adherent  to  the  anterior  capsule  of  the 
crystalline  lens,  the  exudation  in  the  posterior  chamber 
will  press  the  periphery  of  the  iris  forward,  and  give  it  the 
crater-shape,  above  referred  to.  The  pressure  may  be  such 
as  to  bring  the  peripheric  parts  of  the  iris  in  direct  contact 
with  the  posterior  surface  of  the  cornea,  and  if  the  condi- 
tion does  not  soon  heal,  it  induces  atrophy  of  the  tissue  of 
the  iris.  With  the  secretion  of  the  serous  fluid  in  the  an- 
terior part  of  the  vitreous  body  an  increased  emigration  of 
cells  nearly  always  occurs.  In  this  way  larger  agregations 
of  cells  are  formed  in  the  anterior  part  of  the  vitreous  body, 
and  not  infrequently  deposited  upon  the  posterior  capsule 
of  the  crystalline  lens.  In  the  latter  case,  the  exudation  is 
mostly  not  of  a  purely  serous,  but  of  a  sero-fibrinous  charac- 
ter, and  the  cells  upon  the  lens-capsule  are  then  embedded 
in  threads  of  fibrine.  (See  Fig.  48). 


Fig.  48.— Sero-fibrinous  cyclitis.    Amorphus  fibrine,  containing  numerous  round-cells,  lies 
upon  the  posterior  lens-capsule. 

If  the  exudation  is  secreted  by  the  tissue  of  the  ciliary 
body  itself,  it  forces  the  fibres  of  the  ciliary  muscle  apart, 
and  if  this  condition  persists,  they  become  atrophic.  (See 
Fig.  49).     In  rare  cases  only,  we  also  find  the  inner  cellular 


CORPUS  CI  LI  A  RE. 


105 


layers  of  the  ciliary  body,  viz,,  the  uveal  layer  and  the  ciliary 
part  of  the  retina  to  take  an 
active  part  in  the  serous  in- 
flammation. They  then  show 
a  small  degree  of  proliferation. 
If  the  intra-ocular  pressure,  as 
is  not  seldom  the  case,  becomes 
increased  during  the  process, 
these  layers  suffer  accordingly. 
Serous  cyclitis  like  serous 
iritis,  may  recover  without 
leaving  a  trace.  More  fre- 
quently, however,  it  does  not 
pass  off  so  simply.  The  results 
of   complications    to   which    it 

leads,  will  be    discussed  further  ^"'■'*9- -serous  cyclltis.  The  exudation  lies 

in  the  tissue  of  the  ciliary  body  itself,  and 
on.  presses  the  muscular  fibres  apart. 

b.  Cyclitis   Fibrinosa  {Plasticd). 

The  form  of  cyclitis  most  frequently  met  with,  is  the 
fibrinous  or  plastic.  Although  this  form  may  be  found  un- 
complicated, it  is  in  the  majority  of  the  cases  combined,  with 
inflammatory  processes,  in  other  parts  of  the  eye-ball  (espec- 
ially of  the  iris.) 

We  here  again  find  the  blood-vessels  hyperaemic,  and  the 
surrounding  tissue  more  or  less  infiltrated  with  emigrated 
white  blood-corpuscles.  Characteristic  of  this  form  of 
cyclitis,  is  the  fibrinous  exudation.  This  is  at  first  deposited 
upon  the  inner  surface  of  the  ciliary  body  and  zonula  Zinnii. 
In  more  serious  cases  we  find  it  filling  the  whole  of  the  pos- 
terior chamber  and  traversing  the  eye-ball  between  the  iris 
and  the  crystalline  lens,  and  behind  the  latter. 

Doubtlessly  this  exudation  may  at  an  earlier  period  be 
again  absorbed,  and  so  the  serious  results  of  plastic  cyclitis 
may  be  prevented.  The  affection  is,  however,  more  frequent- 
ly observed  to  progress,  and  the  fibrine  becomes  organized. 
After  it  has  been  filled  with  round-cells,  blood-vessels  are 
seen  to  grow  into  it,  coming  from  the  ciliary  body,  and 
sometimes  from  the  peripheral  parts  of  the  retina,  and  thus 


io6 


THE  HUMAN  E  YE. 


the  amorphus  fibrinous  substance  is  gradually  changed  into 
a  delicate  connective-tissue.  In  this  way  the  periphery  of 
the  iris  frequently  becomes  adherent  to  the  ciliary  processes, 
and  the  posterior  chamber  obliterated.  Moreover  this  new- 
formed  connective-tissue  may  cover  the  remainder  of  the 
ciliary  body,  enclose  the  zonula  Zinnii,  and  lying  upon  the 
posterior  capsule  of  the  crystalline  lens,  traverse  the  whole 
of  the  eye-ball.  (See  Fig.  50.) 


Kk;.  50.— Plastic  cyclitis.     Cyclitic  membrane  upon  the  posterior  lens-capsule.    The  pos- 
terior chamber  is  obliterated.     Lens  and  iris  are  pressed  forward. 

This  whole  process  may  go  on  without  materially  altering 
the  uveal  and  retinal  layers  of  the  ciliary  body.  More  fre- 
quently, however,  we  see  that  these  layers  take  an  active 
part  in  the  formation  of  the  cyclitic  membrane,  especially 
the  retinal  part  of  the  ciliary  body.  The  cylindrical  cells  of 
this  layer  proliferate  and  begin  to  grow  out  into  long  spindle- 
shaped  cells,  and  finally  into  long  connective-tissue  fibres. 
This  alteration  of  the  retinal  layer,  always  begins  at  the 
junction  between  pars  plicata  and  pars  nonplicata  of  the 
ciliary  body.  The  parts  lying  more  anteriorly  are  only  in- 
volved later  on  and  never  to  so  great  an  extent.  (See  Fig.  51.) 

Meanwhile  the  cells  of  the  uveal  layer  have  also  under- 
gone proliferation.  The  whole  layer  appears  very  much 
thickened  and  grows  into  the  cyclitic  membrane  in  an  irregu- 
lar way.  We  also  observe,  however,  frequently  a  more  typ- 
ical kind  of  proliferation  of  the  cells  of  the  uveal  layer  in  the 
shape  of  cylindrical  tubes,  which  grow  into  the  cyclitic  mem- 


CORPUS  CILIA  RE. 


107 


brane  and  give  off  branches.     In  longitudinal  and  transverse 
sections,  these  tubes  appear  like  the  glandulce  tubulosa;  or 


Fig.  51. — Plastic  cyclitis.     Shows  how  the  cells  of  the  retinal  layer  of  the  ciliary  body  are 
changed  into  spindle-cells  and  aid  in  the  formation  of  a  cyclitic  membrane. 

the  epithelial  cylinders  of  an  epithelioma.  The  cells  of  these 
tubes  are  either  free  of  pigment  or  pigmented.  Their  shape 
and  arrangement  with  their  branches  have  given  some  authors, 
{Schiess-Gemuseus)  the  idea  that  they  were  blood-vessels, 
whose  walls  were  filled  with  pigment.  Specimens  in  which 
the  blood-vessels  have  been 
injected  with  a  colored 
fluid,  however,  plainly 
show  that  they  are  widely 
different  from  blood-ves- 
sels. They  appear,  as 
stated,  just  like  glands  or 
epithilioma-cylinders.  (See 
Fig.  52). 

Not  all  the  cells  orig- 
inating by  proliferation 
from  the  uveal  layer  are 
pigmented,  and  I  am  even 
convinced  that  the  young  cells  of  this  layer  are  at  first  always 
unpigmented  and  form  their  pigment  only  later  on.     For  this 


Fig.  52.— Plastic  cyclitis.  Tubular  excrescences 
of  the  pigmented  (uveal)  layer  of  the  ciliary 
body. 


io8 


THE  HUMAN  E  YE. 


reason  we  find  in  cycHtic  membranes  also  the  same  tubular 
formations  without  any  pigment  at  all,  which  can  nearly 
always  be  traced  backward  to  a  pigmented  cell-tube  or  the 
uveal  layer  itself.  (See  Fig.  53). 


Fig.  53. — Plastic  cyclitis. 


The  same  tubular  excrescences.    The  younger  ones  as  yet  un- 
pigmented. 


Small  and  large  haemorrhages  are  frequently  found  in  cy- 
clitic  membranes,  and  later  on,  deposits  of  lime  are  very  com- 
mon. Such  membranes  may  furthermore  become  changed 
into  osseous  tissue. 

Cyclitic  membranes,  like  all  new-formed  connective-tissue, 
begin  at  some  period  to  shrink,  and  thus  cause  further  path- 
ological processes  in  the  eye-ball.  At  first  the  nutrition  of 
the  crystalline  lens  is  impaired  to  such  a  degree,  as  to  cause 
the  formation  of  cataract.  Then  the  retraction,  influences 
directly  the  ciliary  body,  and  the  neighboring  part  of  the  cho- 
roid. These  parts  become  detached  from  the  sclerotic,  and 
drawn  inward — and  forward.  It  is  evident,  that  this  detach- 
ment could  not  take  place  if  the  consistency  of  the  vitreous 
body  had  not  before  been  materially  altered,  and  that  it 
must  at  the  same  time  lead  at  least  to  the  peripheral  detach- 
ment of  the  retina.  (See  Fig.  54).  Plastic  cyclitis  may,  also, 
produce  detachment  of  much  larger  parts,  or  even  the  whole 


CORPUS  CILIA  RE.  IO9 

of  the  retina,  and  give  rise  to  chronic  inflammatory  processes 
in  all  parts  of  the  eye-ball,  which  finally  produce  phthisis 
bulbi. 


Fig.  54.— Plastic  cyclitis.    Cylitic  membrane.    Detachment  of  the  ciliary  body. 

c.  Cyclitis  Purulenta  {Parenchymatosd). 

This  form  of  cyclitis  is  observed  especially  after  injuries 
to  the  ciliary  body  itself,  and  as  a  part  of  purulent  panoph- 
thalmitis. Hyperaemia  of  the  blood-vessels  is  always  here 
followed  by  the  rapid  formation  of  pus-cells.  In  the 
earlier  periods,  the  affection  lies  chiefly  in  the  inner  layers  of 
the  ciliary  body,  and  we  find  its  inner  surface  covered  with  a 
fibro-purulent  substance.  Gradually,  however,  the  disease 
spreads,  and  then  later  on  we  find  that  nearly  all  the  layers 
of  the  ciliary  body,  take  an  active  part  in  the  formation  of 
the  pus-cells.  The  last  to  become  involved,  are  the  fibres  of 
the  ciliary  muscle  which,  like  the  nerves,  seem  to  be  very 
resistant.  When  the  disease  has  advanced  so  far,  we  find  the 
whole  of  the  tissue  of  the  ciliary  body  transformed  into  a 
mass  of  round  cells,  between  which  lie  the  free  pigment- 
molecules  and  some  muscular  fibres.  (See  Fig.  55). 

Raab  at  a  recent  date  thought  that  in  a  case  of  purulent 
panophthalmitis  described  by  him,  the  origin  of  the  affec- 
tion was  to  be  found  in  embolism  of  a  ciliary  blood-vessel- 
This,  I  think,  is  for  obvious  reasons  highly  improbable,  and 
has  not  been  observed  by  others. 


1 1  o  THE  H  UMAN  E  YE. 

Purulent  cycHtis  may  as  it  seems,  heal  again  at  an  early 
period.  If  it  does  not,  it  leads  to  the  perfect  destruction  of 
the  involved  tissue. 


Fig.  55. — Purulent  cyclitis. 

In  most  cases  of  purulent  cyclitis,  we  find  the  anterior 
portion  of  the  vitreous  body,  also  filled  with  threads  of  fibrine 
and  pus-cells. 

Except  after  direct  injuries  to  the  ciliary  body,  purulent 
cyclitis  is  but  rarely  a  primary  disease.  If  it  is  the  primary 
affection,  the  inflammation  spreads  very  easily  over  the 
remainder  of  the  uveal  tract.  If  the  iris  becomes  involved, 
we  see  the  formation  of  hypopyon,  if  the  disease  spreads 
upon  the  choroid,  this  is  generally  the  beginning  of  a  puru- 
lent panophthalmitis. 

This  form  of  cyclitis,  like  parenchymatous  iritis,  may  also 
be  found  perfectly  localized  in  the  shape  of  an  accumulation  of 
round  cells,  as  gumma  or  tubercle.  A  gumma  of  the  ciliary 
body  which  I  once  had  the  occasion  to  examine,  consisted 
of  such  an  accumulation  of  round-cells,  which  were  so  crowded 
that  they  began  to  decay  in  the  centre  of  the  little  tumor. 
The  muscular  fibres  were  simply  pushed  aside  and  com- 
pressed. No  blood-vessels  were  found  in  the  tumor.  (See 
Fig.  56.) 

Purulent  cyclitis  may  result  from  plastic  cyclitis.     This  we 


CORPUS  CI  LI  A  RE. 


Ill 


must  assume  to  be  the  case,  whenever  we  find  purulent 
cyclitis  and  a  cyclitic  membrane,  since  the  former  never  leads 
to  the  formation  of  such  membranes. 

i. 


Fig.  56.— Gumma  of  the  ciliary  body.  I.  Iiis.  L.  Lens.  G.  Gumma.  Cm.  Cyclitic  membrane. 


Results  of  Cyclitis. 
Serous  cyclitis  usually  heals  without  leaving  a  trace  ;  but 
the  other  varieties  generally  cause  some  changes  in  the  tissues 
of  the  eye-ball,  which  allow  of  a  certain  diagnosis. 

a.  Cyclitic  Mejttbranes. 
I  already  have  mentioned  the  way  in  which  cyclitic  mem- 
branes are  formed.  It  is  certain  that  the  retinal  layer  of 
the  ciliary  body,  when  proliferating,  is  of  great  importance 
in  these  new-formations,  and  often  even  their  starting  point. 
The  latter  statement  is  proven,  by  the  fact  that  we  not  in- 
frequently find  in  eyes  suffering  from  cyclitis,  the  beginning 
cyclitic  membrane  to  consist  of  nothing,  but  the  proliferated 
cells  of  the  retinal  layer.  They  grow  towards  the  posterior 
pole  of  the  crystalline  lens,  and  I  am  in  the  possession  of 
specimens,  where  this  latter  is  as  yet  perfectly  free.  In  these 
cases  the  cyclitic  product  consequently  does  not  form  a 
membrane,  but  only  a  ring.  In  other  cases,  the  centre  of 
this  ring  is  filled  with  an  amorphous  fibrinous  substance, 
which  is  deposited  upon  the  posterior  capsule  of  the  crys- 
talline lens. 


112 


THE  HUMAN  EYE. 


The  cells  of  the  uveal  layer  of  the  ciliary  body,  are  mostly 
destroyed  during  the  formation  of  a  cyclitic  membrane,  espe- 
cially those  of  the  pars  non-plicata,  and  their  pigment,  being 
freed,  is  with  the  growing  membrane  drawn  towards  the 
centre.  In  other  cases  we  find  besides,  partial  destruction  of 
the  uveal  cells,  a  very  active  proliferation  and  new-formed 
cells,  which  grow  into  the  cyclitic  membrane  arranged  in 
gland-like,  cylindrical  and  tubular  formations.  These  start 
chiefly  from  the  pars  non-plicata  of  the  ciliary  body. 

At  the  same  time  with  these  changes,  we  find  new-formed 
blood-vessels  growing  into  the  cyclitic  membrane,  which  in 
consequence,  is  often  very  vascular.  The  new  blood-vessels 
not  infrequently  give  rise  to  haemorrhages  in  these  mem- 
branes. I  also  mentioned  above,  that  these  membranes  often 
contain  deposits  of  lime,  and  undergo  ossification. 

At  a  certain  stage,  cyclitic  membranes,  like  all  new-formed 
connective-tissues,  begin  to  shrink.  If  the  cyclitis  has  at  the 
same  time  produced  alterations  in  the  posterior  parts  of  the 
eye,  and  especially  in  the  vitreous  body,  this  shrinking  will 
cause  the  ciliary  body  and  the  neighboring  parts  of  the 
choroid  to  become  detached  from  the  sclerotic.  Thus  we 
may  find,  in  a  meridional  section  through  such  an  eye-ball, 
that  two  diametrically  opposite  ciliary  bodies  have  been 
drawn  so  much  towards  the  centre,  that  they  nearly  touch 
each  other.     (See  Fig.  57).     The  same  process  may  further 


KiG.  S7— Plastic  cyclitis  from  an  eye  with  anterior  phthisis.  The  cyclitic  membrane  is  very 
considerably  shrunken,  and  brings  the  ciliary  bodies  nearly  in  contact  with  each  other. 

on  produce  total  detachment  of  the  retina,  which,  however, 
is  generally  preceded  by  an  increase  of  intra-ocular  pressure, 
and  excavation  of  the  optic  nerve  entrance. 


CORPUS  CI  LI  A  RE. 


^3 


b.  Atrophy. 

Although  most  of  the  cases  of  cyclitis,  unless  they  heal, 
lead  to  the  formation  of  a  cyclitic  membrane,  there  are  a 
number  of  cases  in  which  such  a  membrane  is  totally  want- 
ing, and  yet  we  can  judge  from  the  conditions  of  the  ciliary 
body,  that  cyclitis  must  have  existed  during  life.  I  had  in 
one  case  only,  the  occasion  to  find  an  undoubted  hypertro- 
phy, of  the  muscular  tissue 
in  the  ciliary  body  of  an  eye 
which  had  been  injured 
(See  Fig.  58).  It  seems 
therefore  that  cyclitis  may 
cause  hypertrophy  of  the 
muscular  tissue.  Whether 
this  hypertrophy  is  only  a 
spurious  one,  and  leads 
later  on  to  atrophy,  or 
whether  it  may  remain  per- 
sistent, I  cannot  decide. 
In  most  cases  (without  a 
cyclitic  membrane)  we  find 
atrophy  of  the  ciliary  body, 
as   the    result    of    cyclitis.  ^      „    „  ..     .  ,      , 

•'  Fig.  58.— Hypertrophy  of  the  cilary  muscle  in  a 

The    pigmented    and    the  caseofcyciitis. 

retinal  layer,  as  a  rule,  remain  unaltered,  while  all  the  ele- 
ments of  the  parenchyma  of  the  ciliary  body  become  atrophic. 
In  the  most  advanced  cases,  we  find  but  a  very  thin  layer  of 
connective-tissue,  separating  the  uveal  and  the  retinal  layers 
from  the  sclerotic,  as  the  remainder  of  the  ciliary  body.  In 
the  blood-vessels  and  nerves  such  cases  no  longer  exist. 


c.  Staphyloma. 

The  mode  in  which  chronic  cyclitis  may  help  in  the  forma- 
tion of  corneal  and  ciliary  staphylomata,  has  been  explained 
in  Chapter  I. 

B.  Injuries  to  the  Ciliary  Body  and  their  Results. 
Wounds  of  the  ciliary  body  but  rarely  happen  except  the 


114 


THE  HUMAN  EYE. 


part  of  the  sclerotic  covering  it,  has  been  pierced.  The  cih'ary 
body,  may  however,  also  receive  an  injury  from  its  inner 
surface,  after  the  foreign  body  has  perforated  other  parts  of 
the  eye  (mostly  the  cornea,  iris  and  crystalline  lens).  I  found 
furthermore,  in  several  eyes  which  had  been  enucleated  for 
haemophthalmus  subsequent  to  a  contusion,  a  rupture  of 
the  ciliary  body.  In  one  case  the  rupture  beginning  at  its 
outer  surface,  reached  into  the  muscular  tissue.    (See  Fig.  59). 

Ruptures  of  one  or  more  of 
the  blood-vessels  of  the  cil- 
iary body  and  subsequent 
haemorrhagic  infiltration,  of 
its  tissue,  are  not  rare  in 
eyes  having  received  a  con- 
tusion. 

If  the  instrument  by  which 
the  injury  is  inflicted,  has 
pierced  the  sclerotic  and  cil- 
iary body,  the  latter  generally 
prolapses,  and  this  prolapse 
may,  of  course,  be  combined 
with    an    injury    to    the    lens. 

Fig.  59.-Isolated  rupture  of  the  ciliary  body.  (i^'lS,  COmca,  choroid,)  and 
The  eye  was  enucleated  on  account  of  prolapse  of  the  vitrCOUS  body. 
haemophthalmus.     The  tissue  of  the  cil-  ^       u  j         T        1      u  u 

iary  body  was  perfectlyfllled  with  blood.  ->UCn      WOUndS      heal      by      the 

(The  latter  has  not  been  drawn,  to  show  formation       of      a      SCar-tisSUC, 
the  rupture  better.) 

preceded  by  the  exudation  of 
fibrine  into  the  wound-canal.  The  scar-formation  is  as  a  rule 
assisted  in  by  all  of  the  wounded  tissues  (of  course  with  the 
exception  of  the  crystalline  lens).  Later  on  we  then  find  a 
tough  and  frequently  pigmented  band  of  scar-tissue,  uniting 
the  ciliary  body  firmly  with  the  sclerotic.  In  a  number  of 
cases  the  inflammation  will  spread,  and  then  besides  the 
local  changes  we  find  in  the  wound  a  general  plastic,  or  puru- 
lent inflammatory  process. 

If  the  foreign  body  enters  the  ciliary  body  from  the  inte- 
rior of  the  eye-ball,  the  same  conditions  may  be  found,  as 
have  just  been  detailed.  If  the  foreign  body  is  very  small, 
it  may  remain  embedded   in  the  ciliary  body,  and  then    a 


CORPUS  CILIA  RE. 


115 


capsule  of  tough  connective-tsssue  is  gradually  formed  around 
it.  In  the  large  majority  of  cases,  however,  such  a  foreign 
body  will  cause  purulent  cyclitis. 

If  this  local  inflammation  gives  rise  to  a  general  purulent 
inflammation,  the  eye-ball  may  be  perfectly  destroyed.  In- 
juries to  the  ciliary  body  are,  furthermore,  among  the  most 
frequent  causes  of  sympathetic  affections  of  the  fellow-eye. 

C.  Tumors  of  the  Ciliary  Body. 

a.  Myoma. 

Iwanoff  has  so  far  described  the  only  case  of  myoma  of 
the  ciliary  body,  known  in  literature.  The  tumor  of  the  size 
of  a  filbert,  consisted  of  or- 
ganic muscular  fibres  in  the 
parts  nearest  to  the  sclero- 
tic ;  the  inner  parts  con- 
sisted of  connective-tissue. 
It  appears  from  this  de- 
scription rather  doubtful 
whether  this  tumor  can  be 
really  called  a  myoma. 

b.   Sarcoma. 

Sarcoma,  especially  the 
melanosarcoma,  is  the  new- 
formation  most  frequently 
found  to  originate  in  the 
ciliary  body,  (perhaps  the 
only  one).  These  tumors 
come,  however,  as  a  rule, 
under  the  hands  of  the 
anatomist,  when  their  origin 
can  only  be  guessed  at.     It 

,  -  ,  ,  ,  Fig.  60.— Primary  melanosarcoma  of  the  ciliary 

therefore     happened     that  body, 

leucosarcomata  and  melanosarcomata  and  such  sarcomata 
which  were  partly  pigmented,  partly  unpigmented,  have 
been  described  and  said  to  have  originated  in  the  ciliary  body 
without  a  direct  proof,  that  this  was  really  the  case.     I  only 


I  1 5  THE  HUMAN  E  YE. 

once  had  the  occasion  to  examine  a  true  case  of  pigmented 
round-cell  sarcoma  of  the  ciliary  body.  (See  Fig.  60).  The 
whole  of  the  ciliary  body  in  this  case  consisted  of  darkly 
pigmented  round-cells  between  which  no  longer  any  trace  of 
the  muscular  fibres  could  be  found. 

The  mode  in  which  sarcomatous  tumors  of  the  choroid 
spread  over  the  ciliary  body,  will  be  detailed  when  these 
tumors  are  spoken  of.  Primary  sarcoma  of  the  ciliary  body 
is  certainly  of  very  rare  occurrence. 

VI.  Choroidea. 

I.  Normal  Condition. 

The  choroid  consists  of  the  vascular  parenchyma,  an  ex- 
terior coat  of  endothelium  (upon  its  scleral  surface,)  and  the 
lamina  vitrea.  Upon  the  latter,  lies  the  pigmented  (uveal) 
epithelium  which  was  formerly  considered  to  be  part  of  the 
choroid,  but  has  recently  been  assigned  to  the  retina. 
Since  it  suffers  always,  however,  when  the  choroid  is  in  a 
pathological  condition,  it  will  be  spoken  of  after  the  choroid. 

The  parenchyma  of  the  choroid,  like  that  of  the  iris  and 
ciliary  body,  consists  of  a  small  amount  of  connective-tissue, 
some  elastic  fibrillae  and  pigmented  or  unpigmented  cells. 
The  cells  of  the  parenchyma  of  the  choroid  appear  to  be  scat- 
tered equally  over  the  whole  of  its  thickness.  The  pig- 
mented cells  are,  however,  less  numerous  in  the  part  which 
lies  directly  outward  from  the  lamina  vitrea  (the  capillary 
layer).  The  pigmented  cells  of  the  choroid,  have  mostly 
several  long  offsets,  and  accordingly  vary  considerably  in  shape. 
Their  nucleus  is  round  or  oval,  and  free  from  pigment.  The 
pigment,  filling  the  main  body  of  the  cell  and  the  offsets,  is 
granular  and  very  varying  in  its  tint.  While  it  can  hardly 
be  called  brown  in  albinotic  eyes,  it  appears  perfectly  black 
in  the  eyes  of  a  negro,  and  prevents  us  frequently  from  dis- 
cerning the  nucleus  of  these  cells.  The  unpigmented  cells 
are  less  numerous,  and  vary  in  shape,  in  the  same  way  as  do 
the  pigmented  ones.  Some  of  them  are  undoubtedly  lym- 
phatic cells,  others  appear  as  free  nuclei,  without  being  sur- 
rounded by  protoplasma. 

The  blood-vessels  are  a  most  important  part  of  the  paren- 


CHOROIDEA. 


\\^ 


chyma  of  the  choroid.  They  form  two  groups,  viz.,  the 
capillary  blood-vessels,  which  lie  nearer  the  inner,  and  the 
venous  vessels  which  lie  nearer  the  outer  surface  of  the 
choroid.  The  arteries  which  chiefly  conduct  the  blood  to 
this  membrane,  are  the  short  posterior  ciliary  arteries.  After 
having  pierced  the  sclerotic  near  the  optic  nerve  entrance 
and  entered  the  choroid,  they  branch  off  and  these  new 
branches  form  the  capillary  network  of  the  choroid,  which 
ends  with  an  indented  margin  at  the  ora  serrata  {Leber). 
The  long  posterior  and  the  anterior  ciliary  arteries,  send 
small  branches  backwards  to  these  vessels  in  the  choroid. 
The  veins  into  which  the  blood  passes  from  the  capillaries, 
collect  it  into  from  four  to  six  larger  branches,  the  vorticous 
veins,  which  leave  the  eye  through  the  sclerotic.  The  veins 
as  well  as  the  arteries  have  perivascular  sheaths.  Sattler 
has  also  proved  the  existence  of  such  sheaths  around  the 
capillaries,  which,  as  it  appears  from  his  researches,  lie  free  in 
cavities  which  are  in  direct  communication  with  the  perivas- 
cular sheaths  of  the  larger  vessels.  The  same  author  found 
two  endothelial  membranes  separating  the  capillaries  from 
the  veins.  I  have  not  been  able  to  convince  myself  by  my 
own  observation,  of  the  existence  of  these  endothelial  mem- 
branes. Pathological  conditions,  however,  especially  the 
way  in  which  parenchymatous  haemorrhages  may  split  the 
choroid  into  two  layers,  make  it  very  probable,  that  Sattler  s 
statement  is  correct. 

The  parenchyma  of  the  choroid  furthermore,  contains  a 
great  many  nerves.  They  come  from  the  nervi  ciliares  breves 
and  longi,  and  form  a  net-work  of  pale  nerve-fibres  in  the 
choroid,  which  follows  largely  the  arrangement  of  the  blood- 
vessels, and  has  great  many  ganglionic  cells.  The  fibres  of 
this  network  end  in  the  capillary  layer ;  the  manner  of  their 
termination  is,  however,  not  yet  known.  The  ganglionic 
cells  are  very  large,  and  lie  together  in  clusters.  Several 
authors  have  found  organic  muscular  fibres  in  the  choroid. 
The  mode  in  which  the  muscular  fibres  of  the  ciliary  muscle 
end  in  the  choroid,  has  already  been  explained. 

All  that  has  been  said  in  the  previous  chapters  about  the 
laminae  fuscae  and  suprachoroideae,  holds  good  for  the  same 


ii8 


THE  HUMAN  EYE. 


parts  of  the  choroid.  I  may  only  add,  that  the  larger 
branches  of  the  ciliary  nerves,  pass  through  this  layer  of 
fibres,  and  there  form  a  network  with  wide  meshes,  before 
entering  the  parenchyma  of  the  choroid. 

The  choroid  and  sclerotic  adhere  more  firmly  to  each  other 
around  the  optic  nerve-entrance,  where  a  larger  number  of 
blood-vessels  and  fibres  coming  from  the  sclerotic,  enter  the 
choroid.  The  choroid  has  no  more  a  large  round  hole  by 
which  the  optic  nerve  enters  the  eye-ball  in  toto,  than  the 
sclerotic,  as  we  sec  fibres  from  the  so-called  lamina  cribosa, 
enter  the  choroid  and  vice  versa.  The  question  whether 
blood-vessels  from  the  posterior  parts  of  the  choroid,  pass 
over  into  the  optic  nerve-entrance  or  retina,  is  not  yet  con- 
sidered perfectly  settled.  Knapp  has  drawn  such  a  picture 
from  a  diseased  eye,  and  Fig.  6i,  taken  from  a  normal  eye, 

1 


Fig.  6i. — Normal  entrance  of  the  optic  nerve  into  the  eye-ball.    i.  A  blood-vessel  coming 
from  the  choroid  and  entering  the  retina. 

cannot  leave  any  doubt  as  to  the  existence  of  such  blood- 
vessels, although  they  may  not  be  found  in  every  eye. 

The  inner  surface  of  the  choroid  is  covered  by  the  thin 
lamina  vitrea.  This  is  an  elastic  and  perfectly  transparent 
membrane,  upon  which  the  (uveal)  pigmented  epithelium 
lies.  Recently  it  has  been  said  to  have  a  fibrous  structure. 
It  is  not  yet  known,  how  this  membrane  is  united  with  the 
underlying  tissue.  Sattler  found  upon  its  outer  surface  a 
network,  which  he  expressly  says  is  not  formed  by  fibres. 


CHOROIDEA.  I  1 9 

The  pigmented  epithelium,  lying  between  the  choroid  and 
retina,  has  lately,  (first  by  Babuchin)  been  declared  to  be  a 
part  of  the  retina.  J.  Arnold  has,  however,  more  recently 
stated,  that  it  is  not  yet,  perfectly  proven,  that  the  lamina 
pigmenti,  (the  pigmented  epithelium),  is  formed  from  the 
atrophic  posterior  lamella  of  the  secondary  ocular  vesicle  in 
the  foetus,  and  this  conscientious  author  feels  himself  able 
to  state  only,  that  the  lamina  pigmenti,  "replaces"  the  pos- 
terior lamella  of  the  secondary  ocular  vesicle.  This  is  the 
more  important,  as  the  normal  or  pathological  conditions  of 
the  pigmented  epithelium,  are  certainly  found  to  depend 
much  more  upon  the  conditions  of  the  choroid,  than  upon 
those  of  the  retina.  Nearly  every  pathological  condition  of 
the  choroid,  exerts  its  influence  upon  the  pigmented  epithe- 
lium, while  the  most  important  changes  may  happen  in  the 
tissue  of  the  retina,  without  any  alteration  whatsoever,  in  the 
condition  of  the  pigmented  epithelial  cells.  Furthermore,  if 
we  take  the  retina  out  of  a  normal  eye,  these  cells  do  not  ad- 
here to  it,  but  remain  lying  upon  the  choroid. 

Most  recently  it  has  been  found  that  this  layer  of  epithe- 
lial cells  secretes  the  retinal  purple,  {Kuehne,  Boll).  It  repre- 
sents therefore  a  kind  of  gland,  lying  between  retina  and 
choroid,  as  an  independent  organ. 

The  cells  forming  this  epithelial  layer  are  mostly  hexa- 
gonal. They  are  united  with  each  other  by  a  structureless 
cementing  substance,  and  form  one  single  layer  of  flattened 
epithelium.  Their  nuclei  are  round  and  unpigmented;  their 
protoplasm  is  filled  with  granular  pigment.  The  pigmenta- 
tion varies  considerably  in  the  cells  of  one  and  the  same  eye. 
In  the  eyes  of  negroes,  the  pigment  is  as  a  rule  very  dark, 
but  it  rarely  altogether  hides  the  nucleus. 

In  some  eyes,  especially  those  of  old  people,  the  cement- 
ing substance  between  these  cells  is  found  to  be  much  broader 
and  thicker,  and  if  the  cells  are  carefully  removed,  a  tough 
network  remains  lying  upon  the  lamina  vitrea  of  the  choroid, 
the  meshes  of  which  are  filled  by  the  cells.     (See  Fig.  62). 

Nearly  all  of  the  recent  authors  on  this  subject,  have  de- 
scribed and  drawn  very  fine  and  long  offsets  which  the  cells 
of  the  pigmented  epithelium  are  said  to  send  in  between  the 


1 20  THE  HUMAN  E  YE. 

rods  and  cones  of  the  retina.  They  are  said  to  be  either  pig- 
mented or  unpigmented.  Schwalbe,  one  of  these  authors, 
states,  however,  that  in  the  human  eye  they  produce  only  a 
very  loose  union  between  the  retina  and  the  pigmented 
epitheHum.  I  must  confess,  that  I  have  searched  in  the  hu- 
man eye  in  vain  for  these  offsets.  In  eyes  taken  from  corpses 
which  have  begun  to  decay,  a  condition  similar  to  the  granu- 
ular  offsets,  drawn  by  Schwalbe,  is  frequently  seen  ;  in  fresh 
eyes,  however,  or  eyes  put  into  Mueller  s  hardening  fluid 
when  perfectly  fresh,  I  cannot  find  them. 

Cells  with  two  or  more  nuclei  are  rare  among  the  normal 
pigmented  epithelial  cells,  but  there  are  always  a  number  of 
small  cells,  which  are  probably  of  a  more  recent  date. 

2.  Pathological  Conditions. 
A.  Pathological  Changes  of  the  Pigmented  Epithelium. 
It  seems  to  me  that  before  we  go  on  to  a  description  of 
the  different  kinds  of  inflammation  the  choroid  is  subject  to, 
this  is  the  proper  place  to  speak  of  the  pathological  changes 
observed  in  the  pigmented  epithelium.  Nearly  every  patho- 
logical process  in  the  choroid  involves  this  layer,  and  we 
would  thus  be  forced  to  frequently  repeat  the  same  ;  on  the 
other  hand,  there  are  a  number  of  pathological  changes  ob- 
served in  the  pigmented  epithelium  which  are  peculiar  to  it, 
and  more  or  less  independent  of  any  affection  of  the  choroid. 
The  most  common  pathological  alteration  the  cells  of  the 
pigmented  epithelium  undergo,  is  that  they  lose  their  regular 
shape  and  uniformity  in  size.  The  new  forms  are  very  mani- 
fold, and  the  pigment  lies  mostly  in  the  periphery  of  the  pro- 
toplasma,  in  these  cells.  It  seems  also,  as  if  the  pigment 
could — so  to  speak,  be  secreted  by  one  and  taken  up  by 
another  cell  in  its  neighborhood.  The  latter  then  appears 
perfectly  black.  Later  on  round  or  oblong,  light  (empty  or 
filled  ?)  structures  are  seen  inside  the  cells,  which  by  some 
authors  are  considered  to  be  colloid-globules,  by  others  to  be 
vacuolae.  If  the  cells  are  altered  in  such  a  way,  the  cement- 
ing substance  is  found  to  be  either  hardened,  and  to  remain 
adherent  to  the  lamina  vitrea  (See  Fig.  62),  or  to  have  ap- 
parently altogether  disappeared. 


CHOROIDEA. 


121 


Combined  with  these  alterations,  we  very  frequently  find 
between  the  pigmented  epithelial  cells,  round  or  oval,  trans- 
parent, hard  bodies  which  ad- 
here to  the  lamina  vitrea. 
These  have  by  English  au- 
thors, received  the  name  of 
colloid  excrescences  of  the 
lamina  vitrea,  and  have  been 
often  described  as  such.  There 

U^,,,«Tr^^        ^^      ^^ C     i-X^^i-  Fig.  62.— Thickened   and  hardened  intercel- 

IS,       however,  no      proof     that        i,,ar   substance  from  the  pigmented  epi- 

these     bodies  consist    really     of       theliallayer,  lying  upon  the  lamlna  vitrea 

1,     .  ,           1      ,  ,,      .                          of  the  choroid;  i,  containing  lime. 

colloid  substance;  their  per- 
fect resistance  to  all  chemical  agents,  and  their  hardness 
would  on  the  contrary  tend  to  prove  that  they  are  not  of  a 
colloid  nature.  In  transverse  sections,  they  resemble  very 
much  the  corpora  arenacea  of  the  coats  of  the  brain.  (See 
Fig.  63).     The   fact,  that    they  lie  upon   the  lamina  vitrea, 


Fig.  63.— Vitreous  bodies  upon  the  lamina  vitrea  of  the  choroid;  i,  containing  lime. 

and  are  only  found,  where  the  pigmented  epithelium  is 
altered  in  the  manner  above  referred  to,  seems  to  prove  that 
their  formation  is  caused  by  these,  and  Mayer  has  recently 
tried  to  show  that  these  bodies  are  really  secreted  by  the 
cells  of  the  pigmented  epithelium.  I  must  agree  with  him 
in  considering  this  the  most  probable  way  in  which  they 
are  formed,  although  I  have  seen  a  great  number  of  speci- 
mens, in  which  it  appeared  as  if  they  were  the  result  of  a 
degenerative  process  of  the  cells  themselves.  While  the 
smaller   sized   vitreous    bodies  are  generally  covered    by   a 


122 


THE  HUMAN  EYE. 


continous  layer  of  pigmented  epithelial  cells,  part  of  which 
are  new-formed,  these  cells  are  gradually  destroyed  as  the 
vitreous  bodies  grow  larger  and  coalesce.  This  may  be 
simply  the  consequence  of  the  pressure,  but  it  is  possible 
also,  that  the  protoplasma  of  the  cells  is  the  material,  by 
which  these  vitreous  bodies  grow.  Through  these  changes, 
the  pigment  molecules  become  free,  and  seem  to  be  taken 
up  by  the  more  or  less  normal  cells  which  surround  the  basis 
of  the  vitreous  bodies,  and  which  now  appear  perfectly 
dark,  and  sometimes  in  a  state  of  proliferation. 

It  has  often  been  stated  that  these  bodies  are  peculiar  to 
old"  age.  This  may  in  the  majority  of  cases  really  be  so  ; 
they  are,  however,  found  in  the  eyes  of  young  individuals 
also,  for  I  found  an  immense  quantity  of  them  once  in  the 
eye  of  a  boy  twelve  years  of  age. 

Later  on  amorphous  lime  is  frequently  deposited  inside 
these  vitreous  bodies  and,  in  spite  of  their  hardness,  it  cannot 
be  impossible  for  cells  to  penetrate  into  them,  as  they  may 
become  organized  in  the  form  of  osseous  tissue.  (See 
Fig.  64). 


Fig.  64. — Formation  of  osseous  tissue  in  the  vitreous  bodies  of  the  lamina  vitrea  choroidea:. 

An  undue  and  pathological  new-formation  of  cells,  is  not 
infrequent  in  the  pigmented  epithelial  layer.  It  is  seen  in 
nearly  all  of  the  cases  of  choroiditis  and  we  have  already 
spoken  of  it,  when  describing  the  changes  caused  by  cyclitis. 
The  new-formed  cells  are,  (as  stated  already  by  Virchoiv)  at 
first  nearly  always  free  from  pigment.  They  are,  however, 
as  it  seems,  able  to  form  their  pigment  at  any  time  them- 
selves. The  new-formation  of  cells  may  produce  a  simple 
thickening  of  the  pigmented  epithelium,  by  superposing 
layer   after  layer  of  new   cells.     The   formation    of  tubular 


CHOROIDEA. 


123 


offsets,  similar  to  the  epithelial  cyHnders  of  an  epitheliomata, 
appears,  however,  to  be  more  frequent.     (See  Fig.  65). 


Fia.  65.— Tumor-like  new-formation  of  pig^mented  and  unpigmented  celUcylinders.  starting 
from  the  uveal  layer  of  the  ciliary  body  and  neighboring  choroid. 

An  affection  of  the  retina  of  great  clinical  importance,  is 
caused  by  such  an  hyperplasia  of  the  pigmented  epithelium, 
without  any  pathological  change  in  the  choroid,  vis.^  pig- 
mentary retinitis.  In  such  cases  the  tubular  offsets  of  the 
pigmented  epithelium  are  partly  pigmented,  partly  unpig- 
mented, and  grow  into  the  retina,  after  having  first  destroyed 
its  outer  layers.  In  the  retina,  these  foreign  substances 
cause  a  chronic  interstitial  inflammation,  which  leads  to 
hypertrophy  of  the  connective-tissue,  and  to  destruction  of 
the   nervous   elements.     (See  Fig.  66).     Furthermore,    new 


124 


THE  HUMAN  E  YE. 


connective-tissue    is    formed  in  the   perivascular  sheaths    of 
the    retinal    blood-vessels  (perivasculitis)  and    these  become 


Fir..  66. — Pigmentary  retinitis.  Pigmented  cell  cylinders  going  over  in  such  cylinders  with- 
out pigment.     Blood-vessel  changed  into  connective-tissue. 

gradually  obliterated.  It  seems  that  this  process  often 
begins  in  the  peripheral  parts  of  the  retina  ;  in  a  case  which 
I  described  recently,  it  involved  only  a  zone  of  retinal  tissue, 
ten  millimetres  in  width,  and  equally  distant  from  the  ora  ser- 
rata  and  the  optic-nerve  entrance.  That  the  peripheric  vision 
is  at  first  impaired  in  cases  of  this  affection,  does  not  depend 
alone  on  the  disease  usually  beginning  in  the  peripheral  parts 
of  the  retina,  but  also  upon  the  diminished  quantity  of 
nutritive  fluids,  furnished  to  these  parts. 

We  shall  see  later  on  that  some  forms  of  choroiditis,  may 
be  followed  by  a  very  similar  kind  of  pigmentation  of  the 
retina.  The  genuine  pigmentary  retinitis  is,  however,  a  sec- 
ondary affection,  caused  without  any  affection  of  the  choroid 
proper,  by  the  primary  pathological  new-formation  of  cells  of 
the  pigmented  epithelial  layer. 


CHOROIDEA.  125 

During  the  process  of  this  disease,  the  pigmented  cells 
may  enter  the  perivascular  sheath  of  a  retinal  blood-vessel. 
(See  Fig.  6"/).  The  primary  disease  is,  however,  not  one  of 
the  blood-vessels,  as  has  been  stated  by  former  authors. 


Fig.  67. — Pigmentary  retinitis.  Pigment  in  the  perivascular  sheatli  of  a  retinal  blood-vessel. 

The  cells  of  the  pigmented  epithelium  may  undergo  fatty 
degeneration.  This  seems  to  be  most  frequent  in  eyes  with 
total  detachment  of  the  retina.  Such  cells,  are  then  often 
transformed  into  aggregations  of  round  fat-granules  (Koern- 
chenkugeln),  which  may  or  may  not  contain  some  pigment 
molecules. 

B.  Choroiditis  and  its  Results. 
The  large  number  of  different  forms  of  choroiditis  which 
the  clinicists  treat  of,  are  anatomically  summed  up  under  the 
following  three  heads,  viz.,  i.  serous  (serous-fibrinous),  2.  fibrin- 
ous (plastic)  and  3.  purulent  (parenchymatous  choroiditis). 
This  distinction  is  made  according  to  the  products  of  the 
inflammatory  process.  These  are  exuded  either  into  the 
tissue  of  the  choroid  itself,  or  into  the  parts  lying  to  the  inner 
side  of  this  membrane,  (the  pigmented  epithelium,  retina  and 
vitreous  body),  and  we  find  therefore  most  cases  of  cho- 
roiditis complicated  with  inflammatory  processes  in  other 
parts  of  the  eye-ball,  (especially  the  pigmented  epithelium, 
the  retina  and  vitreous  body). 

a.  Choroiditis  Serosa  {sero-fibrinosd). 

Serous  choroiditis,  which  is  not  infrequently  met  with, 
has  recently  been  perfectly  identified  with  glaucoma.     This 


126  THE  HUMAN  EYE. 

Standpoint  has  been  chiefly  accepted  by  Schmit-Rimpler 
and  von  Wecker  in  Gmfe  and  ScemiscJi  s  Cyclopaedia. 
Although,  as  will  be  shown  further  on,  it  is  possible 
that  glaucomatous  symptoms  result  from  serous  choroiditis, 
we  do  not  always  find  serous  choroiditis  when  there  is  glau- 
coma. Whoever  has  had  the  occasion  to  examine  a  number 
of  glaucomatous  eyes,  will  know  that  it  is  impossible  in  most 
of  the  cases,  to  detect  any  change  in  the  condition  of  the 
choroid. 

Serous  choroiditis,  which  I  therefore  do  not  identify  with 
glaucoma,  is  ushered  in  by  hyperaemia  of  the  blood-ves- 
sels, especially  the  veins  of  the  choroid.  This  hyperaemia 
may  concern  the  whole  of  the  choroid,  or  be  more  or  less 
localized.  I  found  it  several  times  to  be  confined  to  one 
vorticous  vein,  or  even  only  to  a  large  branch  of  one.  This 
hyperaemia  is  followed  by  the  exudation  of  a  serous,  some- 
times a  sero-fibrinous  fluid.  In  hardened  specimens,  it  ap- 
pears that  this  fluid  is  but  very  rarely  exuded  into  the  tissue 
of  the  choroid  itself,  which  is,  however,  no  proof  that  the 
conditions  are  not  different  in  life.  The  serous  exudation  is 
mostly  found  inwards  from  the  choroid,  between  the  lamina 
vitrea  and  the  pigmented  epithelium,  or  between  the  pig- 
mented epithelium  and  the  retina,  or  between  retina  and 
vitreous  body,  (especially  in  their  posterior  half),  or  in  the 
vitreous  body  itself.  Furthermore,  I  frequently  found  in 
cases  of  serous  or  sero-fibrinous  choroiditis,  small  round  and 
oval  cavities  in  the  outer  granulur  layer  of  the  retipa,  filled 
with  a  sero-fibrinous  fluid,  the  formation  of  which  may  be 
caused  directly  by  the  disease  of  the  choroid,  before  a  sec- 
ondary affection  of  the  retina  can  be  developed. 

Some  more  recent  authors  have  proven  that  chemical,  not 
histological  alterations  in  the  tissues  of  the  eye,  are  the  chief 
cause  of  the  serous  exudation.  If  this  exudation  is  not  soon 
absorbed,  it  will  produce  different  pathological  alterations, 
in  the  condition  of  the  tissues  according  to  the  place  where  it 
lies.  It  may  lead  to  partial  or  total  detachment  of  the  retina 
(with  or  without  the  pigmented  epithelium),  from  the  choroid, 
or  to  detachment  of  the  vitreous  body  from  the  retina,  or  it 
may  simply  produce  liquefaction  of  the  vitreous  body.     The 


CHOROIDEA.  127 

consistency  of  the  latter  must,  of  course,  have  been  consider- 
ably altered,  before  either  it  or  the  retina  can  become  de- 
tached, and  especially  in  cases  of  total  detachment  of  the 
retina,  the  vitreous  body  must  either  have  been  totally  lique- 
fied or  condensed.  The  liquefaction  of  the  vitreous  body  is, 
however,  found  too,  without  being  accompanied  by  detach- 
ment. I  must  state  here  that  every  detachment  of  the 
retina  is  not  caused  by  serous  choroiditis.  There  are  quite  a 
number  of  factors,  which  may  come  into  play  in  detaching 
the  retina  from  the  choroid,  which  have  already  been  partially 
and  will  be  more  fully  described  further  on. 

The  increased  production  of  serous  fluid  within  the  eye- 
ball, especially  when  the  means  of  exit  are  pathologically 
altered,  or  totally  obliterated,  may  so  increase  the  intra-ocu- 
lar  pressure,  that  we  find  later  on,  all  the  symptoms  of  glau- 
coma, including  excavation  of  the  optic  nerve.  This  is  espe- 
cially found  in  eyes  suffering  from  some  kind  of  staphyloma 
(except  posterior  sclero-choroidal  staphyloma). 

Sometimes  we  find  the  number  of  wandering  cells  in  the 
choroid  considerably  increased  in  cases  of  serous  choroiditis. 
There  is,  however,  in  the  choroid  at  least  no  sign  of  cell- 
proliferation  to  be  detected.  The  vitreous  body  also  is 
usually  filled  with  a  larger  number  of  cells,  and  the  serous 
exudation  contains  them.  The  cells  of  the  pigmented  epithe- 
lium are  partially  proliferating,  partially  undergoing  a  regres- 
sive metamorphosis.  If  the  exudation  remains  for  a  long 
time  lying  in  the  same  place,  we  frequently  find  crystals  of 
cholesterine  formed,  and  lime  deposited  in  it.  The  former 
appear  always  in  the  well  known  tablets  ;  the  lime  is  amor- 
phous. The  formation  of  vitreous  bodies  upon  the  lamina 
vitrea  of  the  choroid,  is  frequently  met  with  in  such  cases. 

h.  Choroiditis  Fibrinosa  {plasticd). 

Plastic  choroiditis  never  attacks  the  whole  choroid,  but 
appears  in  numerous  small  patches,  which  may  by  con- 
fluence grow  larger.  Hyperaemia  of  the  choroid  in  this  form 
of  inflammation,  is  followed  by  a  fibro-cellular  exudation 
at  first  into  the  tissue  of  the  choroid  itself.  (See  Fig.  68). 
We  then  find  in  such  a  place,  a  round  or  oval  accumulation 


128 


THE  HUMAN  EYE. 


of  fibrinous   substance    involving   mostly  the  whole   thick- 
ness of  the  choroid,  and  filled  with  and  surrounded  by  round- 


Fig.  68. — Plastic  choroiditis.    Fibro-cellular  exudation  in  the  tissue  of  the  choroid. 

cells.  If  the  process  of  exudation  goes  on,  the  lamina  vitrea 
is  perforated,  and  the  fibrinous  substance  may  remain 
under  the  thus  detached  pigmented  epithelium.  In  the 
majority  of  cases,  however,  this  layer,  too,  is  perforated,  and 
the  exudation  enters  the  tissue  of  the  retina.  This  fibrinous 
substance,  is  later  on  transformed  into  connective-tissue, 
which  at  some  period  will  begin  to  shrink.  If  the  fibrine  has 
been  exuded  only  into  the  tissue  of  the  choroid,  we  find, 
later  on  unpigmented,  round  and  oval  patches,  which  are 
very  thin  and  consist  of  connective-tissue,  without  either 
blood-vessels  or  cellular  elements.  In  these  cases,  also  where 
the  exudation  has  not  directly  involved  the  pigmented  epi- 
thelium, we  find  it  later  on  changed,  and  the  cells  covering 
the  patch  of  exudation  lose  their  pigment  and  may  be  totally 
destroyed,  which  latter  condition  is  caused  by  the  pressure 
exerted  upon  them,  as  well  as  by  impairment  in  their  nutri- 
tion. Their  pigment  having  thus  been  freed,  is  taken  up  by 
the  cells  in  the  periphery  of  the  patch  of  exudation,  which 
consequently  appear  abnormally  dark.  If  the  exudation  has 
once  perforated  the  lamina  vitrea,  the  retina  is  always  sure 
to  suffer,  although  to  a  greatly  varying  degree.  The  rods 
and  cones  alone  may  be  destroyed,  and  the  pigmented  epi- 
thelium adhere  to  the  retina.  If  the  pigmented  epithelium 
has  been  perforated  by   the  fibrinous  exudation,  the  latter 


CHOROIDEA. 


129 


will  enter  the  retina  and  there  produce  a  local  interstitial 
inflammation.  When  the  fibrinous  substance  has  been  trans- 
formed into  connective-tissue  and  begins  to  shrink,  retina 
and  choroid  will  thus  become  firmly  adherent  to  each  other. 
(See    Fig.    69).     Moreover,  the  pigmented  epithelium    cells 


Fig.  69.— Plastic  choroiditis.    Adhesion  between  retina  and  choroid. 

may  begin  to  proliferate  and  so  to  produce  either  a  thick- 
ening of  this  layer,  or  form  the  above  described  tubular  ex- 
crescences. If  the  latter  be  the  case,  the  retina  becomes 
pigmented  in  the  manner  we  have  seen,  in  the  so  called  pig- 
mentary retinitis.  (See  Fig  70).  All  these  processes  are  clin- 
ically called  chorio-retinitis. 


Fig.  70. — Plastic  choroiditis.    Pigmentation  of  the  retina. 

In  rare  cases  the  fibrine  may  be  exuded  directly  upon  the 
inner  surface  of  the  lamina  vitrea,  i.  e.  between  lamina  vitrea 
and  pigmented  epithelium. 

Retraction  of  the  new-formed  connective-tissue,  uniting 
retina  and  choroid  in  the  manner  above  referred  to,  may 
cause  the  neighboring  parts  of  the  retina,  to  become  de- 
tached from  the  pigmented  epithelium. 

The  disease  may  in  the  first  stages,  heal  by  absorption  ; 
in  most  of  the  cases,  however,  it  progresses  and  leads  to  the 
local   new-formation    of  connective-tissue   and  atrophy  just 


I30 


THE  HUMAN  E  YE. 


detailed.  Vitreous  bodies  upon  the  lamina  vitrea,  are  fre- 
quently observed  in  eyes  so  affected. 

There  are  a  number  of  clinically  distinct  forms  of  cho- 
roiditis, which  anatomically  all  belong  under  this  head,  viz., 
choroiditis  disseminata,  atrophica,  exudativa,  areolaris,  cho- 
rio-retinitis  disseminata  and  chorio-retinitis  centralis.  The 
latter  name  means  that  the  affection  is  confined  to  the  region 
of  the  macula  lutea. 

The  small  patches  of  exudation  may  lie  very  close  to  each 
other,  and  finally  by  coalescing,  form  very  large  ones.  The 
original  patches  are,  however,  always  comparatively  small. 

c.  Choroiditis  Purulenta  {Parenchymatosd). 

The  characteristic  feature  of  purulent  choroiditis,  is  the 
enormous  emigration  and  new-formation  of  cells,  in  the  paren- 
chyma of  the  choroid,  which  may  lead  to  perfect  destruction 
of  this  membrane.  The  affection  is  in  most  of  the  cases  a  dif- 
fuse one,  and  concerns  the  whole  of  the  choroid.  We  also  find, 
however,  local  round-cell  accumulations,  like,  abscesses  at  the 
same  time  with  the  diffuse  affection.  In  the  very  advanced 
cases,  the  whole  of  the  structure  of  the  choroid,  is  simply 
represented  by  an  innumerable  mass  of  round-cells.  (See 
Fig.  71).     Knapp  says  that  the  formation  of  pus  always  be- 


FiG.  71. — Purulent  choroiditis. 

gins  in  the  capillary  layer.  This  is  not,  however,  without 
exception,  the  case.  All  of  the  different  elements  constitu- 
ting the  tissue  of  the  choroid,  even  the  muscles,  take  an 
active   part    in   the  formation    of  round-cells.     The  lamina 


CHOROIDEA. 


131 


vitrea  is  frequently  perforated,  and  thus  the  pus  enters  into 
the  parts  lying  inwards  from  the  choroid.  The  pigmented 
epithelium  begins  to  proliferate,  and  the  retina  becomes  de- 
tached. The  vitreous  body  appears  very  soon  pervaded  by 
a  large  number  of  pus-cells.  The  formation  of  pus  may  also 
involve  the  inner  layers  of  the  sclerotic,  and,  when  progressing, 
lead  to  perforation  of  this  membrane.  The  purulent  inflam- 
mation seldom  remains  confined  to  the  choroid,  but  generally 
spreads  over  the  other  parts  of  the  uveal  tract,  or  over  all  the 
other  membranes  of  the  eye-ball,  that  is,  it  produces  a  puru- 
lent panophthalmitis. 

This  form  of  acute  purulent  (diffuse)  choroiditis,  is  either 
of  spontaneous  origin,  or  is  caused  by  an  injury.  The  spon- 
taneous form  is  frequently  called  "  metastatic  "  choroiditis, 
especially  when  found  in  individuals  suffering  from  pyaemia. 
It  is,  however,  not  yet  undoubtedly  proven,  that  in  such 
cases,  the  choroiditis  must  really  be  considered  as  a  metastic 
affection.  Raab,  who,  as  I  already  stated,  found  an  embolus 
in  a  ciliary  artery,  considered  this  to  be  proof  of  the  metas- 
tatic character  of  this  variety  of  choroiditis. 

Tubercles  of  the  choroid,  are  local  parenchymatous  affec- 
tions. Although  such  tubercles  have  frequently  been  exam- 
ined with  the  microscope,  the  similar  gummatous  affection, 
which  from  clinical  observation  may  doubtless  happen,  does 
not  seem  to  have  so  far  been  examined  histologically.  The 
tubercles  have  nothing  peculiar  in  the  choroid.     They  are  an 


Fig.  7a.— Tubercle  of  the  choroid. 

accumulation  of  round-cells  in  the  parenchyma  of  this  mem- 
brane, and  frequently  contain  giant-cells.  (See  Fig.  72).  They 
may  be  found  in  all  parts  of  the  choroid,  single  or  coalescing. 


132 


THE  HUMAN  EYE. 


Acute  purulent  choroiditis,  almost  always  take  on  a  chro- 
nic form.  Secretion  of  pus  ceases,  the  blood-vessels  are  all 
destroyed,  and  formation  of  connective-tissue  ensues.  We 
may  thus  have  the  opportunity  of  examining  such  eyes  at  a 
period,  when  the  tissue  replacing  the  choroid,  is  six  or  more 
times  as  thick  as  this  membrane  appears  in  the  normal  condi- 
tion. This  thickening  is,  however,  not  persistent,  but  fol- 
lowed by  shrinking  of  the  new-formed  tissue,  and  perfect 
atrophy  of  the  eye-ball. 

The  nerves  may  be  found  unaltered,  even  in  the  most 
violent  forms  of  purulent  choroiditis.  When  the  process  has, 
however,  led  to  perfect  atrophy  of  the  choroid,  we  usually 
look  for  them  in  vain. 

Besides  acute  parenchymatous  choroiditis,  which  goes 
over  into  the  chronic  form,  we  sometimes  observe  a  purulent 
choroiditis,  which  is  from  the  beginning  of  a  chronic  charac- 
ter. This  frequently  leads  to  the  deposition  of  lime,  in  the 
parenchyma  of  the  choroid,  and  to  the  formation  of  osseous 
tissue.  We  have  seen  above,  that  the  formation  of  osseous 
tissue  may  take  place  in  the  vitreous  bodies  lying  upon  the 
lamina  vitrea  of  the  choroid,  and  I  am  inclined  to  look  upon 


Fig.  73. — Osseous  tissue,  with  marrow  in  the  choroid. 

these  bodies  as  being  more  frequently  the  origin  of  the 
osseous  tissue,  than  we  suspect,  especially  when  it  is  found 
lying  upon  the  inner  surface  of  the  lamina  vitrea. 


CHOROIDEA.  133 

The  formation  of  bone  in  the  choroid  in  the  beginninij, 
usually  takes  place  in  its  inner  layers  {Knapp).  Later  on, 
the  whole  choroid  may  be  found  thus  altered.  The  osseous 
shell,  formed  in  such  a  manner,  never  reaches  farther  an- 
teriorly, than  to  the  ciliary  body.  In  its  posterier  part,  it 
is  usually  perforated  by  the  optic  nerve  or  retina.  The 
osseous  tissue  differs  in  no  way  from  the  normal  osseous 
tissue,  and  in  rare  cases  may  even  contain  cavities  filled  with 
marrow.     (See  Fig.  jt,). 

Since  chronic  parenchymatous  choroiditis  usually  leads 
to  chronic  inflammatory  processes  of  the  eye-ball,  which 
cause  the  new-formation  of  connective-tissue,  we  have  to  look 
upon  it  as  the  chief  cause  of  the  shrinking  of  the  whole 
eye-ball,  known  under  the  name  of  phthisis  bulbi,  and  of  con- 
sequent sympathetic  affections  in  the  fellow-eye. 

The  Results  of  Choroiditis. 

a.  Detachment  of  the  Retina  and  Vitreous  Body. 

In  consequence  of  serous  choroiditis,  we  may  find,  as 
above  stated,  the  retina  detached  from  the  choroid,  and  the 
vitreous  body  from  the  retina.  Detachment  of  the  retina 
may  be  total  or  only  partial.  We  always  find  in  these  cases 
(when  the  detachment  has  been  caused  by  serous  choroiditis) 
more  or  less  exudation  between  the  retina  and  choroid, 
which,  in  spite  of  the  means  used  to  harden  the  eye-ball, 
remains  sometimes  perfectly  fluid, or  may  become  gelatinous. 

It  is  most  probable  that  during  life,  the  retina  too,  is 
saturated  by  this  serous  fluid,  and  isoedematous.  Some  small 
round  or  oval  cavities  in  the  external  granular  layer,  filled 
with  a  sero-fibrinous  fluid,  were  all  I  could  find  in  hardened 
eyes  to  prove  this.  The  retina,  too,  clearly  suffers  from 
some  other  pathological  processes,  which  will  be  detailed 
presently.  With  the  retina,  a  number  of  cells  of  the  pig- 
mented epithelial  layer,  or  even  large  parts  of  this  layer  may 
be  detached.  Vitreous  bodies  from  the  lamina  vitrea  may 
also  adhere  to  the  detached  retina,  and  in  one  case,  where  I 
found  osseous  tissue  in  the  detached  retina,  this  had  most 
probably  originated  in  such  detached  vitreous  bodies. 


134  THE  H  UMA  N  E  YE. 

The  vitreous  body  may  be  found  detached  from  the 
retina  by  serous  fluid,  whether  this  membrane  is  removed 
from  the  choroid  in  the  manner  just  stated,  or  whether  it 
is  in  its  normal  position.  The  vitreous  body  then  appears 
condensed  and  pressed  forward  towards  the  ciliary  body  and 
the  crystalline  lens. 

b.  Liquefaction  of  the   Vitreous  Body. 
This  condition  will  be  detailed  further  on  in  Chapter  X. 

c.  Glaucomatous  Excavation  of  the  Optic  Papilla. 

The  alterations  caused  in  the  "  head  *'  of  the  optic  nerve, 
and  later  on  in  the  retina,  in  consequence  of  increased  intra- 
ocular pressure,  will  be  referred  to  in  Chapters  VII  and 
VIII. 

d.  Atrophy ;  Synechia  between  Retina  and  Choroid,  and 
Pigmentation  of  the  former. 

If  atrophy  of  the  choroid  is  diffuse,  it  has  been  caused  by 
a  purulent  (parenchymatous),  if  it  is  found  in  patches,  by  a 
fibrinous  (plastic)  choroiditis.  The  atrophic  patches  caused 
by  plastic  choroiditis,  are  round  or  oval,  or  when  several  have 
coalesced,  very  manifold  in  shape.  In  a  plain  view,  the  pig- 
mented epithelium  is  wanting  upon  them,  and  they  them- 
selves appear  free  from  pigment  and  blood-vessels.  The  pig- 
mented epithelium  cells  surrounding  the  patches  are  consid- 
erably darker  than  the  rest.  In  transverse  sections,  these 
atrophic  patches  appear  very  considerably  thinner  than  the 
surrounding  parts  of  the  choroid. 

As  above  stated,  the  retina  is  very  frequently  found  to 
adhere  firmly  to  the  atrophic  patches  in  the  choroid.  In 
such  places  it  is  very  thin,  and  drawn  towards  the  choroid. 
During  this  process,  the  rods  and  cones  become  destroyed, 
and  thus  the  pigmented  epithelium  may  grow  into  the 
retina,  and  cause  it  to  become  pigmented  in  a  manner  closely 
resembling  the  conditions  seen  in  cases  of  pigmentary  retini- 
tis. The  pigment  may  even  enter  the  lymphatic  sheaths  of 
the  blood-vessels,  as  I  must  state  contrary  to  vo7i  Weckers 
opinion. 


CHOROIDEA. 


135 


If  atrophy  of  the  choroid  has  been  caused  by  chronic 
parenchymatous  choroiditis,  it  nearly  always  concerns  the 
whole  of  this  membrane.  We  find  this  condition  chiefly  in 
shrunken  (phthisical)  eye-balls.  During  this  process,  the 
choroid  may  become  firmly  adherent  to  the  sclerotic,  and,  if 
the  retina  was  involved,  choroid  and  retina  may  also  be  found 
to  adhere  so  firmly  to  each  other,  that  they  can  no  longer 
be  separated.  In  some  cases,  if  there  is  not  pigment  enough 
left  to  mark  the  line  of  demarcation,  it  may,  even  with  the 
microscope,  be  impossible  to  distinguish  between  the  re- 
mains of  the  two  membranes.  In  advanced  cases,  nearly  all 
the  blood-vessels  are  perfectly  destroyed,  and  the  same  is  the 
case  with  the  nerves. 

e.  Ossification. 

The  formation  of  osseous  tissue  in  the  choroid,  is  a  com- 
paratively frequent  result  of  chronic  parenchymatous  cho- 
roiditis. Most  authors  consider  that  this  ossification  origi- 
nates in  a  fibrino-plastic  exudation  {Knapf).  It  is  true,  that 
we  often  find  in  cases  of  ossification  of  the  choroid,  a  fibrino- 
plastic  exudation  lying  upon  the  inner  surface  of  the  choroid, 
and  partially  ossified.  I  am,  however,  of  the  opinion  that 
the  ossification,  when  lying  upon  the  inner  surface  of  the 
choroid,  very  frequently  has  for  its  origin,  the  vitreous  bodies 
of  the  lamina  vitrea.  on  the  other  hand  I  do  not  deny  that 
it  sometimes  originates  in  the  new-formed  tissue  consequent 
upon  plastic  choroiditis,  to  which  we  have  an  analogue 
in  the  formation  of  osseous  tissue  in  cyclitic  membranes. 
The  osseous  tissue  within  the  parenchyma  of  the  choroid, 
however,  seems  to  me,  to  be  formed  chiefly  during  a  chronic 
parenchymatous  choroiditis.  The  whole  of  the  choroid  is 
sometimes  found  to  be  changed  into  osseous  tissue,  so  that 
it  can  only  be  recognized  by  the  folded  lamina  vitrea,  which 
is  generally  preserved. 

It  is  certainly  a  strange  fact  that,  in  spite  of  the  similar- 
ity in  the  structure  of  the  choroid  and  iris,  as  yet  no  ossifica- 
tion has  been  found  in  the  latter.  The  osseous  formations 
described  upon  the  posterior  surface  of  the  iris,  originated  in 
cyclitic  productions  in  that  place. 


136 


THE  HUMAN  E  YE. 


f.  Staphyloma. 

The  manner  in  which  chronic  choroiditis  may  aid  in  the 
formation  of  a  scleral  staphyloma,  has  been  sufficiently  de- 
tailed in  Chapter  II. 

C.  Injuries  to  the  Choroid  and  their  Results. 

The  peculiar  fact,  that  a  contusion  of  the  eye-ball  may 
cause  a  more  or  less  isolated  rupture  of  the  choroid,  has  not 
yet  been  satisfactorily  explained.  It  is  greatly  to  be  regretted, 
that  up  till  now  no  such  case  seems  to  have  been  histologically 
examined  and  described.  It  appears  from  clinical  observa- 
tion, that  the  rupture  chiefly  concerns  the  inner  layers  of  the 
choroid.  The  pigmentation  of  the  retina,  frequently  formed 
in  the  surrounding  of  the  rupture,  is  most  probably  the 
result  of  a  simultaneous  rupture  of  the  outer  layers  of  this 
membrane,  by  which  the  pigment  is  enabled  to  grow  into  it. 

If  the  injury  only  leads  to  the  rupture  of  some  blood- 
vessel of  the  choroid,  a  larger  or  smaller,  parenchymatous 
haemorrhage  will,  of  course  ensue,  according  to  the  size  of 
the  blood-vessel.  The  blood  may  be  so  distributed  in  the 
tissue,  that  this  appears  haemorrhagically  infiltrated ;  or  it 
may  split  the  choroid  into  two  layers  and  force  them  con- 
siderably apart.     (See   Fig,  74).     These  haemorrhages  later 


Fig.  74.— rareuchymatous  haemorrhage  splitting  the  choroid  into  two  layers,  caused  by  con- 
tusion of  the  eye-ball. 

on  undergo  fatty  degeneration,  and  become  gradually  ab- 
sorbed, leaving  behind  them  a  more  or  less  atrophic  tissue, 
filled  with  crystals  of  haematoidine. 


CHOROIDFA. 


-^17 


Foreign  bodies  striking  the  choroid  must,  of  course,  have 
pierced  the  sclerotic  or  the  retina  before  reaching  it,  and 
such  injuries  therefore  always  produce  complicated  condi- 
tions. If  the  sclerotic  and  choroid  only  have  been  injured, 
the  latter  generally  prolapses  into  the  wound  of  the  sclero- 
tic, and  the  two  membranes  heal  together  by  means  of  a  local 
plastic  inflammation.  The  sclerotic  then,  as  a  rule,  appears 
pigmented  around  the  wound.  If  the  retina,  choroid  and 
sclerotic,  have  been  wounded  from  the  interior,  all  the 
wounded  parts  show  this  local  plastic  inflammation.  Since, 
however,  the  choroid  has  the  most  reproductive  power  of 
the  three,  we  frequently  find  a  pigmented  granulation-tissue 
growing  from  it  through  the  retina  into  the  vitreous  body. 
(See  Fig.  75),     Later  on,  this  granulation-tissue  shrinks,  and 


Fig.  75. — Granulation-tissue  starting  from  the  wounded  choroid. 

we  find  pigmented  scar-tissue,  by  which  the  membranes  are 
firmly  united  with  each  other.  The  retina  surrounding  the 
scar  is  nearly  always  pigmented,  and  all  the  parts  next  to  the 
scar,  contain  crystals  of  haematoidine. 

I  have  never  found  a  foreign  body  to  be  encapsuled  in 
the  choroid  alone. 

The  inflammation  caused  by  such  injuries  remains,  how- 
ever, but  seldom  a  localized  one.  It  generally  leads  to  puru- 
lent choroiditis,  or  even  to  panophthalmitis.  Moreover,  the 
simple  scar,  as  described  above,  may  become  stretched,  and 
cause  the  formation  of  a  traumatic  staphyloma  of  the  scle- 
rotic. 

It  appears,  that  injuries  have  in  rare  cases  become  the 
starting  point  for  the  formation  of  malignant  tumors  in  the 
choroid. 


1 38  THE  HUMAiY  E  YE. 

Injuries  to  this  membrane  may  also  finally  produce  sym- 
pathetic affections  of  the  other  eye. 

D.  Tumors  of  the  Choroid. 

a.  Cystoid  Formations. 

Only  once  I  found  cystoid  formations  in  the  choroid. 
They  were  situated  in  the  peripheric  part  of  this  membrane, 
and  formed  a  number  of  large  round  and  oval  cavities,  which 
(in  the  hardened  eye),  appeared  to  be  empty.  They  had  a 
membrana  propria,  and  an  endothelial  coating.  They  proba- 
bly originated  from  the  lymphatic  sheaths  of  a  blood-vessel, 
and  would  then  be  analogous  to  lymphangiectasia.  (See  Fig. 
76). 


Fig.  76.— Cystoid  formation  in  the  choroid. 

b.  Granuloma. 

After  injuries  to  the  choroid,  when  abscess-like  round 
cells  accumulations  in  this  membrane  have  perforated  the 
lamina  vitrea,  we  sometimes  find  granulation  tissue  starting 
from  the  parenchyma  of  the  choroid.  Such  a  granuloma  is 
never  very  large,  and  it  may  either  detach  the  retina  from 
the  choroid,  or  if  this  membrane  too  has  been  perforated,  it 
may  grow  through  it  into  the  vitreous  body.  These  tumors 
seem  at  a  later  period  to  be  always  changed  into  tough 
connective-tissue,  and  thus  to  form  a  simple  scar. 

Leber  showed  to  the  meeting  of  oculists  at  Heidelberg,  in 
1878,  specimens  of  granuloma  of  the  choroid,  from  an  individ- 
ual who  had  suffered  from  granulated  eye-lids  (trachoma). 

c.  Sarcoma. 
The  most  frequent  new-formations  of  the  choroid,  are  the 


CHOROIDEA.  139 

sarcomata.  Knapp  has  written  a  very  extensive  book  on  this 
subject,  and  to  him  belongs  the  merit  of  having  placed  our 
knowledge  with  regard  to  choroidal  tumors,  on  a  more  exact 
basis.  Since  its  appearance,  only  very  little  has  been  added 
to  this  chapter.  There  are  pigmented  and  unpigmented  sar- 
comata of  the  choroid.  The  unpigmented  ones  are,  however 
rarely  altogether  free  from  pigment.  The  cells  of  these  tu- 
mors are  either  round  or  spindle-shaped.  The  pigmented 
sarcomata  consist  mostly  of  large  cells,  and  the  latter  show  a 
varying  degree  of  pigmentation.  Sometimes  the  cells  are  so 
crowded  with  pigment  molecules,  that  it  is  impossible  to  see  a 
nucleus.  While  the  unpigmented  round-cell  sarcomata  consist 
chiefly  of  small  cells,  and  are  frequently  very  vascular,  the 
unpigmented  spindle-cell  sarcomata  are  tougher,  less  vascular, 
and  of  a  more  fibromatous  character. 

According  to  Knapp,  the  unpigmented  sarcomata  take 
their  origin  from  the  outer  layers  of  the  choroid,  which  are 
more  fibrous,  while  the  pigmented  ones  spring  chiefly  from 
the  inner,  especially  the  capillary  layer.  It  is  as  yet  not 
known  whether  and,  if  so,  in  what  way,  the  pigmented 
epithelium  may  help  in  the  formation  of  these  tumors. 

The  sarcomata  of  the  choroid  may  be  very  vascular,  and 
contain  cavernous  spaces  of  varying  size.  The  latter,  the 
so-called  teleangiectatic  form  of  sarcoma,  seems  to  be  more 
frequently  found  in  unpigmented  than  in  pigmented  tumors, 
and  is  often  combined  with  haemorrhages  in  the  surrounding 
tissue.  In  the  small-celled  sarcoma  more  so  than  in.  any 
other  variety,  fatty  degeneration  of  the  cells  is  often  seen. 
Also  chalky  deposits  have  been  described  in  sarcomatous 
tumors.  Knapp,  however,  has  never  seen  them,  and  mine  is 
the  same  experience.  It  is  therefore  likely  that  the  tumors 
in  which  they  were  seen,  were  retinal  and  not  choroidal  new- 
formations. 

Intra-ocular  enchondroma  of  the  eye  has  been  described 
by  Knapp.  I  had  occasion  to  describe  two  cases  of  choroidal 
sarcoma  with  formation  of  cartilage  tissue,  and  having  exam- 
ined the  tumor  described  by  Knapp,  I  am  strongly  inclined  to 
believe  that  it  belonged  to  the  same  class.  Hyaline  cartilage 
appears  in  the  choroidal  sarcoma  in  shape  of  islets  which 


I40 


THE  HUMAN  EYE. 


generally  lie  in  the  neighborhood  of  larger  blood-vessels. 
These  islets  are  surrounded  by  a  capsule  of  connective-tissue. 
Although  it  is  certainly  not  impossible  that  the  cartilage  is 
formed  by  the  transformation  of  the  formative  cells  of  a  sar- 
coma, my  opinion,  based  upon  anatomical  facts,  is,  that  the 
remains  of  the  vitreous  body  inclosed  in  the  sarcoma,  are  its 
real  starting  point.  (See  Fig.  77, 


Fig.  77. — From  a  chondrosarcoma  of  the  choroid,  i.  Sarcoma-cells.  2.  Cartilage-tissue  ;  in 
its  centre,  (3)  remains  of  the  vitreous  body  changed  into  delicate,  myxomatous  tissue. 
4.  Connective-tissue  surrounding  the  cartilage-tissue. 

The  formation  of  osseous  tissue  in  intra-ocular  sarcomata, 
is  but  rarely  observed.  I  have  only  once  come  across  such 
a  specimen.  (See  Fig.  78). 

Cowell  described  a  cysto-sarcoma  of  the  choroid.  The 
cysts  were  filled  with  a  transparent  fluid,  and  were  probably 
formed  by  the  incarcerated  exudation,  or  parts  of  the  vitreous 
body. 

Besides  these  forms  of  choroidal  tumors,  a  great  many 
others  have  been  described  by  other  writers,  analogues  of 
which  the  more  modern  authors  have  not  seen.  I  consider 
it  therefore  better  not  to  mention  them  at  all,  as  their  ex- 
istence must  be  proven  by  more  exact  anatomical  observa- 
tions. 

During  its  growth  the  retina  may  for  a  long  time  remain 
adherent  to  the  choroidal  sarcoma.     In  most  cases  this  mem- 


CHOROIDEA.  141 

brane  is,  however,  detached  by  exudation.     In  the  later  stages 
the  retina  may  altogether  disappear. 


Fig.  78. — Osseous  tissue  formed  in  a  sarcomatous  tumor  of  the  choroid. 

The  new-formation  later  on  spreads  upon  the  ciliary  body 
and  iris,  either  simply  by  continuous  growth  or  by  infection. 
The  elements  of  the  tumor  may  furthermore  invade  the 
sclerotic  and  optic  nerve.  If  the  sclerotic  becomes  perforated 
by  the  tumor,  or  the  optic  nerve  is  destroyed,  extra-ocular 
tumors  are  formed. 

During  the  growth  of  the  new-formation  the  nutrition  of 
the  anterior  parts  of  the  eye  must  needs  become  greatly  im- 
paired, and  the  intra-ocular  pressure  increased.  This  pro- 
duces the  formation  of  abscesses  in  the  cornea,  and  some- 
times perfect  destruction  of  this  membrane.  This  is  another 
way,  in  which  the  tumor  may  grow  out  of  the  eye-ball. 

Finally,  the  new-formation  leads  to  metastases,  which  are 
of  the  same  structure  as  the  primary  tumor  in  other  organs. 
Such  metastatic  tumors  are  found  chiefly  in  the  liver ;  they 
may  appear  also  in  the  lungs,  pleura,  intestines,  kidneys, 
spleen,  brain  and  other  organs. 


VII. 

NERVUS   OPTICUS. 
I.  Normal  Condition. 

Although  this  book  is  meant  to  deal  only  with  the  tis- 
sues of  the  eye-ball  itself,  it  would  be  impossible  to  speak  of 
the  intra-scleral  part  of  the  optic  nerve,  and  to  utterly  disre- 
gard the  parts  of  the  nerve  which  lie  farther  back.  In  thus 
transgressing  my  programme,  I  do  so  in  order  to  aid  in  a  bet- 
ter understanding  of  the  relations  of  the  intra-ocular  part 
of  the  optic  nerve.  We  will  speak  in  the  following  pages  of 
the  optic  nerve  near  and  within  the  sclerotic  and  choroid, 
and  of  the  papilla  nervi  optici,  or  the  so-called  "  head  "  of 
the  optic  nerve.  The  latter  I  do  not  consider  as  Schwalbe 
does,  to  constitute  a  part  of  the  retina,  although  it  lies  in- 
wards from  the  choroid. 

When  speaking  of  the  optic  nerve,  we  have  to  make  a 
distinction  between  its  outer  and  its  inner  sheath,  and  the 
nerve  itself. 

The  outer  sheath  of  the  optic  nerve  consists  of  two  parts, 
viz.,  the  dura  mater  and  the  arachnoid.  The  inner  sheath, 
which  lies  close  to  the  optic  nerve,  is  analogous  to  the  pia 
mater. 

The  dura  mater  sheath  is  by  far  the  thickest  of  the  three. 
It  passes  directly  over  into  the  sclerotic,  and  its  structure  is 
essentially  the  same  as  that  of  the  latter  membrane.  It  con- 
sists of  tough  connective-tissue  fibrillae,  which,  according  to 
Schwalbe,  in  its  outer  layers  run  mostly  in  a  longitudinal,  in 
its  inner  layers  in  a  circular  direction.  Near  the  junction 
with  the  sclerotic  we  find  only  longitudinal  fibres.  Elastic 
fibrillae  are  also  frequently  found  in  the  dura  mater  sheath. 
Between  these  fibres  lie  a  number  of  flat  cells  (Schwalbe) 
which  are  very  thin,  have  an  oval  nucleus  and  an  nucleolus. 
If  not  isolated,  they  appear  like  spindle-cells.  The  inner 
surface  of  this  sheath  is  lined  with  a  single  layer  of  delicate 


NERVUS  OPTICUS. 


143 


endothelial  cells.  It  contains,  moreover,  numerous  blood- 
vessels and  nerves. 

The  arachnoid  sheath  which  lies  comparatively  close  to 
the  dura  mater  sheath,  is  a  very  thin  membrane.  It  consists 
chiefly  of  a  network  of  fine  connective-tissue  fibres,  in  the 
meshes  of  which  lie  endothelial  cells.  Thin  connective- 
tissue  trabeculae  unite  these  two  sheaths,  while  we  find  much 
thicker  ones  connecting  the  arachnoid  sheath  with  the  pia 
mater  sheath. 

The  pia  mater  sheath  which  closely  surrounds  the  optic 
nerve  itself,  has  a  tough  outer  and  a  delicate,  loose  inner 
layer.  It  also  contains  a  number  of  elastic  fibres,  and  is  lined 
on  its  outer  surface  with  a  single  layer  of  delicate  endothelial 
cells.  Such  cells  are  furthermore  found  to  adhere  to  the 
trabeculae  uniting  the  outer  and  inner  sheaths  with  each 
other.  The  numerous  blood-vessels  found  in  the  pia  mater 
come  from  those  of  the  dura  mater,  and  returning  branches 
of  the  short  ciliary  arteries. 

The  peculiar  network  of  connective-tissue  which  en- 
sheathes  the  nerve  fibre  bundles  of  the  optic  nerve,  takes  its 
origin  from  the  pia  mater  sheath. 

The  trabeculae  of  this  network  form  comparatively  small 
meshes  in  which  the  numerous  nerve  fibre  bundles  appear 
embedded.  In  transverse  sections  the  connective-tissue  is 
seen  to  form  rings  (alveoli)  of  different  size.  In  longitudinal 
sections  we  see  the  trabeculae  regularly  arranged  in  longitu- 
dinal and  transverse  directions  and  intersecting  each  other. 
The  fibrillae  of  this  connective-tissue  are  closely  attached  to 
each  other,  and  it  has  therefore  the  sclerotic  appearance, 
which  we  mentioned  in  connection  with  the  fibres  of  the 
ligamentum  pectinatum  iSchwalbe). 

The  optic  nerve  is  pierced  near  or  just  at  its  axis  by  a 
small  amount  of  delicate,  loose  connective-tissue,  in  which 
the  central  retinal  artery  and  vein  are  embedded. 

The  nerve  itself  is  by  the  connective-tissue  divided  into 
a  very  large  number  of  small  bundles  of  varying  size  and 
shape. 

The  nerve  fibre  bundles  of  the  optic  nerve  consist  of 
double  contoured  nerve  fibres,  which  vary  in  thickness,  and 


144  ^^^  HUMAN  E  YE. 

lack  a  Schwann  s  sheath  {Schwalbe).  These  fibres  are  united 
with  each  other  by  neuroglia,  which  consists  of  a  homogen- 
eous matrix  and  numerous  cells.  The  oval  short  nuclei  of 
the  latter  in  hardened  and  stained  specimens  are  readily  dis- 
tinguished from  those  of  the  connective-tissue.  In  longitu- 
dinal sections  they  appear  arranged  in  rows  in  a  longitudinal 
direction.  The  cells  are  of  a  varying  shape,  but  are  mostly 
flat  and  must  be  considered  as  endothelial  cells. 

At  the  optic  nerve  entrance,  the  dura  mater  sheath  and 
the  arachnoid  sheath,  now  firmly  united  into  one,  pass 
directly  over  into  the  sclerotic  and  make  part  of  its  outer 
layers.  The  pia  mater  sheath  enters  the  eye  with  the  optic 
nerve  until  it  has  reached  the  choroid.  It  then  is  united  with 
the  inner  layers  of  the  sclerotic,  and  helps  in  the  formation 
of  the  lamina  cribrosa. 

While  the  space  between  the  pia  mater  and  arachnoid  thus 
becomes  obliterated  behind  the  sclerotic,  the  wider  space  be- 
tween the  arachnoid  and  pia  mater  (subarachnoidal,  subvagi- 
nal,  intervaginal  space)  can  be  traced  into  the  sclerotic. 
Sometimes  it  even  appears  to  be  enlarged  within  this  mem- 
brane, and  in  certain  (chiefly  myopic)  eyes,  it  is  seen  to  bend 
at  right  angles  and  thus  (in  transverse  sections)  to  divide  the 
sclerotic  into  two,  generally  unequal  parts. 

The  optic  nerve  itself  becomes  much  thinner  after  having 
entered  the  sclerotic.  The  cause  of  this  is  found  in  the  fact 
that  the  double-contoured  nerve  fibres  are  changed  into  non- 
medullated  ones.  I  would  here  like  to  point  out  a  difference 
in  the  manner  in  which  this  change  of  the  nerve  fibres  takes 
place  in  very  short  (hypermetropic)  and  in  very  long  (myopic) 
eye-balls,  which  as  far  as  I  know  has  not  yet  been  mentioned 
elsewhere.  While  in  short  eyes  the  nerve  becomes  only 
very  gradually  thinner,  and  this  attenuation  begins  already 
somewhat  behind  the  sclerotic,  it  takes  place  in  a  very  abrupt 
manner  in  long  eyes,  and  just  where  the  thin  sclerotic  and 
choroid  surround  the  nerve.  This  is  caused  by  the  different 
manner  in  which  the  double-contoured  nerve  fibres  go  over 
into  non-medullated  ones.  In  the  short  eyes  the  boundary 
line  between  the  two  appears  in  a  longitudinal  section  through 
the  axis  of  the  nerve  in  the  shape  of  a  funnel,  the  basis  of 


NERVUS  OPTICUS. 


H5 


Fic.  79 — Shows  how  the  double-contoured  nerve- 
fibres  of  the  optic  nerve  changed  into  non. 
medulatedones  in  an  hypermetropic  eye. 


which  lies  within  the  outer  lamellae  of  the  sclerotic,  while  its 
apex  lies  considerably  farther  backward.  (See  Fig.  79).  In 
long  eyes  the  transforma- 
tion of  the  nerve  fibres 
takes  place  in  such  a  way,  ^^B 
that  the  boundary  line  is 
straight  or  convex  towards 
the  front  of  the  eye-ball, 
and  lies  just  where  sclerotic 
and  choroid  surround  the 
nerve,  that  is,  within  the 
lamina  cribrosa.  (See  Fig. 
80).  I  am  at  a  loss  to  explain  this  fact ;  it  is,  however,  also 
in  macroscopical  specimens  so  evident,  that  it  invites  further 
investigations. 

After  the  pia  mater  has  joined  the  sclerotic,  the  latter 
surrounds  the  nerve  directly,  and  we  see  numerous  thick 
trabeculae  of  connective-tissue  spring  from  it,  traverse  the 
optic  nerve  and  thus  form,  what  is  called,  the  lamina 
cribrosa.  In  the  formation  of  the  latter  the  choroid  also 
aids.  In  longitudinal  sections  of  these  parts,  we  see  the 
longitudinal  connective-tissue  trabeculse  become  gradually 
thinner ;  at  the  same  time  the  number  and  thickness  of 
the  transverse  ones  is  so  considerably  increased,  that  while 


Fig.  80. — Shows  how  the  double-contoured  nerve-fibres  ot  the  optic  nerve  are  changed  into 
non-medulated  ones  in  a  myopic  eye. 

we  find  in  a  part  of  the  optic  nerve  lying  farther  backward, 
but  of  the  same  size,  perhaps,  half  a  dozen  transverse  trabe- 
culae, we  find  here  twenty,  thirty  and  more.  In  transverse 
sections  of  this  region  we  see  furthermore,  that  the  meshes 
between  the  connective-tissue  trabeculae  are  much   smaller 


146  THE  HUMAN  EYE. 

and  more  numerous,  than  in  those  parts  of  the  nerve  which 
lie  farther  back. 

The  blood-vessels  of  the  optic  nerve  come  from  those  of 
its  sheaths  and  from  the  central  retinal  vessels.  They  form 
a  capillary  network  between  the  nerve  fibre  bundles  to  which 
small  branches  are  added  within  the  lamina  cribrosa,  which 
come  from  Hallers  "  vascular  ring "  formed  by  the  short 
ciliary  arteries. 

The  subdural  and  the  subarachnoidal  spaces  are  continua- 
tions of  the  intra-cranial  spaces  of  the  same  name,  and  must 
be  considered  as  lymphatic  spaces.  Through  minute  fissures 
in  the  sclerotic,  they  are  in  communication  with  the  supra- 
choroidal  space  ;  they  furthermore  communicate  with  fissures 
in  the  nerve  itself,  and  through  these  with  the  perivascular 
spaces  in  the  retina,  which  we  will  describe  later  on. 

When  the  optic  nerve  has  passed  through  the  lamina 
cribrosa,  its  fibres  are  bent  nearly  at  right  angles,  and  before 
entering  the  retina,  f^rm  the  so-called  papilla  nervi  optici. 
Most  of  these  nerve  fibres  take  a  radiary  direction,  and  ac- 
cording to  Liebreich,  a  larger  number  run  upward  and  down- 
wards than  towards  the  sides  of  the  eye-ball.  The  fibres  bend 
gradually,  and  in  the  papilla  are  accompanied  by  a  great  many 
connective-tissue  elements,  which  later  on  partly  disappear 
and  partly  enter  the  retina.  The  manner  in  which  the  nerve 
fibres  enter  this  membrane,  causes  the  papilla  to  have  a  more 
or  less  central  depression,  which  is  surrounded  by  walls  differ- 
ing in  height  according  to  the  distribution  of  the  nerve  bun- 
dles entering  the  retina. 

The  papilla  contains  a  large  number  of  capillary  blood- 
vessels and  within  it  both  the  central  retinal  artery  and  vein 
are  divided  into  branches.  Injections  into  the  lymphatic 
sheaths  show  in  the  papilla  a  number  of  fissures  radiating 
from  its  centre  towards  the  retina. 

2.  Pathological  Conditions. 

We  shall  speak  only  of  the  pathological  conditions  of 
that  part  of  the  optic  nerve  which  lies  close  to  the  eye-ball 
and  within   it.     We  shall  also  find  here  that  the  affections 


NERVUS  OPTICUS. 


H7 


called  by  numerous  clinical  names  become  but  few,  when 
anatomically  considered.  The  nerve-tissue  proper  is  no 
more  prone  to  independent  inflammation  here  than  else- 
where and  in  many  forms  of  the  affections,  clinically  de- 
scribed as  neuritis  optica,  the  nerve-tissue  as  such,  takes  but 
little  or  no  part  at  all  in  the  inflammatory  process. 

Anatomical  researches  have  proven  beyond  doubt,  that 
every  affection  causing  an  increase  of  intra-cranial  pressure 
(especially  tumors  of  the  brain)  may  exert  a  direct  influence 
upon  the  optic  nerve,  especially  its  intra-ocular  part  by  caus- 
ing dropsical  enlargement  of  the  intervaginal  space,  and 
serous  exudation  into  the  nerve,  consequent  upon  the  former. 
Furthermore,  we  may  observe  an  inflammatory  process  of  the 
sheaths  which  leads  to  obliteration  of  the  intervaginal  space 
and  consequent  inflammatory  processes  in  the  connective- 
tissue  of  the  optic  nerve.  Nearly  as  frequent  as  dropsical 
enlargement  of  the  sheaths  we  meet  with  primary  inflamma- 
tory processes  in  the  connective-tissue  of  the  nerve,  especially 
the  papilla.  The  rarest  affection  is  certainly  an  independent 
inflammation  of  the  nervous  fibres  themselves. 

We  shall  describe  in  the  following  pages,  i.  oedema  of 
the  optic  nerve  and  papilla  ;  2.  inflammation  of  the  sheaths 
of  the  optic  nerve  ;  3.  interstitial  and  4.  parenchymatous 
neuritis. 

a.  CEdema  of  the  Optic  Nerve  and  Papilla. 

As  stated  above,  various  causes,  producing  an  increase  of 
intra-cranial  pressure,  may  lead  to  the  filling  of  the  inter- 
vaginal space  with  an  abnormal  quantity  of  serous  fluid,  and 
thus  gradually  distent  it.  The  increase  of  pressure  in  the 
intervaginal  space,  of  course,  can  not  exist  for  any  length  of 
time  without  influencing  the  condition  of  the  optic  nerve. 
As  described,  the  intervaginal  space  communicates  with  the 
lymphatic  canals  within  the  optic  nerve,  and  we  must  there- 
fore soon  also  find  an  increased  pressure  within  these.  They 
appear  sometimes  very  considerably  enlarged,  and  are  seen 
as  fissures  and  small  cavities  within  the  connective-tissue 
trabeculae.    The  connective-tissue  fibres,  by  which  the  sheaths 


148 


THE  HUMAN  EYE. 


of  the  optic  nerve  are  united,  and  which  run  through  the  in- 
tervaginal  space  become  atrophied,  in  rare  cases  hypertro- 
phied. 

These  changes  in  and  around  the  optic  nerve  cause  com- 
pression of  its  blood-vessels,  thus  leading  again  to  serous 
transudation  from  that  source,  and  to  oedema  of  the  papilla 
optici.  The  latter  is  characterized  by  hyperaemia,  especially 
of  the  veinous  blood-vessels,  and  later  on  we  find  serous  fluid 
between  the  swollen  fibres.  Wide  canals  and  cavities  sever 
the  fibres,  which,  in  hardened  specimens,  appear  empty.  It 
seems  that  neither  the  serous  fluid  in  the  intervaginal  space 
nor  within  the  papilla,  contains  a  large  quantity  of  cellular 
elements.     (See  Fig.  8i). 


y      1  ''"- ^ 

Fig.  8i.— CEdema  of  the  intervaginal  space  and  optic  papilla,    i.  The  enlarged  mtervagma- 
space.    3.  Spaces  in  the  optic  papilla  filled  with  serum. 

This  oedema  of  the  optic  nerve  and  papilla  may  again 
disappear  as  soon  as  the  increased  pressure  becomes  reduced, 
and  the  normal  conditions  may  be  reestablished.  During  the 
existence  of  the  oedema,  haemorrhages  into  the  optic  nerve 
and  papilla  frequently  occur.  If  the  disease  progresses, 
atrophy  of  the  optic  nerve  fibres,  and  hypertrophy  of  the 
connective-tissue  will  be  the  result.  The  affection  evidently 
must  also  influence  the  retina.  At  a  later  period  we  find 
this  membrane  also  in  a  state  of  serous  imbibition,  and  its 
nerve  fibres  swollen  ;  furthermore,  we  meet  with  hypertrophy 
of  the  connective-tissue,  haemorrhages  and  fatty  metamor- 
phosis, especially  of  the  ganglionic  cells. 


NEK V us  OPTICUS. 


149 


An  active  inflammation  of  the  parts  thus  affected,  seems 
to  be  of  rare  occurrence. 

b.   Vaginitis  Nervi  Optici. 

As  we  may  find  each  of  the  meninges  of  the  brain  sepa- 
rately inflamed  (pachymeningitis  and  leptomeningitis),  there 
are  probably  also  separate  inflammatory  processes  in  the  outer 
and  inner  sheath  of  the  optic  nerve.  Since,  however,  the 
earliest  stages  of  vaginitis  optici  have  as  yet  not  been  satis- 
factorily examined,  this  is  not  proven.  But  there  is,  no 
doubt  left,  that  a  fibrinous  or  purulent  inflammation  of  the 
meninges  may  cause  the  same  affection  in  the  sheaths  of 
the  optic  nerve,  and  influence  the  conditions  of  the  latter  ac- 
cordingly. 

Fibrinous  vaginitis  is  combined  with  a  high  degree  of 
hyperaemia  in  the  sheaths.  The  intervaginal  space  at  first 
contains  a  large  amount  of  amorphous  fibrine  mixed  with 
lymphatic  cells.  Later  on,  it  is  found  to  be  altogether  filled 
with  fibrine  and  cells,  and  the  latter  begin  to  proliferate. 
Thus  the  exudation  is  gradually  organized,  the  proliferation 
of  the  endothelial  cells  of  the  intervaginal  space  aids  mate- 
rially in  this  process.  Blood-vessels  are  seen  to  spread  into 
this  fibro-cellular  substance,  and  soon  we  find  it  transformed 
into  connective-tissue.  The  intervaginal  space  in  this  way 
becomes  perfectly  obliterated.     (See  Fig.  82).     During  the 


Fig.  8j.— Fibrinous  vaginitis  of  the  optic  nerve,    i.  Intervaginal  space  obliterated  by  new- 
formed  connective-tissue.    Optic  nerve  atrophic. 

progress    of  this    transformation,    haemorrhages    frequently 
occur. 

While  these  changes  take  place  in  the  intervaginal  space. 


I50 


THE  HUMAN  E  YE. 


the  optic  nerve  and  papilla  cannot  remain  unaltered.  Their 
connective-tissue  is  more  and  more  infiltrated  with  round- 
cells,  and  numerous  new  blood-vessels  are  formed.  Then  the 
connective-tissue  becomes  hypertrophied,  the  nervous  ele- 
ments atrophy  and  simply  fade  away.  During  these  changes 
haemorrhages  frequently  take  place  within  the  optic  nerve 
and  papilla. 

Besides  the  fibrinous  vaginitis  optici,  there  is  a  purulent 
form,  which  is,  however  rare,  and  probably  only  observed  in 
consequence  of  purulent  meningitis.  In  such  cases  we  find 
the  sheaths,  as  well  as  the  intervaginal  space  filled  with 
round-cells,  and  later  on  also  the  optic  nerve  and  papilla. 
It  seems  that  in  consequence  of  an  early  death  in  these  affec- 
tions, further  changes  have  not  been  observed. 

c.  Interstitial  Neuritis. 

Probably  the  most  frequent,  certainly  the  most  important 
affection  of  the  optic  nerve,  is  inflammation  of  the  inter- 
stitial connective-tissue.  Although  such  an  interstitial  neu- 
ritis may,  as  we  have  seen,  arise  from  oedema  of  the  nerve 
and  inflammation  of  its  sheaths,  it  is  very  frequently  a  pri- 
mary disease.  The  inflammatory  process  involves  the  neu- 
roglia as  well  as  the  connective-tissue  trabeculae,  which  sever 
the  nerve  fibre  bundles. 

A  high  degree  of  hyperaemia  of  the  optic  nerve  and  papilla 
is  followed  by  an  enormous  cell-infiltration  and  proliferation 
in  the  connective-tissue.  (See  Fig.  83).  The  connective- 
tissue  trabeculae  appear  thicker,  and  in  consequence  of  the 
large  number  of  new  cells  in  them  and  the  neuroglia,  the 
whole  of  the  nerve  appears  in  fine  sections  infiltrated  with 
round-cells.  (See  Fig.  84).  The  infiltration,  however,  con- 
cerns the  nerve  fibres  themselves  but  very  slightly,  if  at  all. 
Later  on,  a  large  number  of  new-formed  blood-vessels  fill  the 
papilla,  which  in  consequence  of  these  changes  is  sometimes 
enormously  swollen.  The  blood-vessels  of  the  nerve  as  well 
as  those  of  the  papilla  are  frequently  found  to  be  surrounded 
by  a  mantle  of  round-cells. 

These  new-formed  cells  are  gradually  changed  into  connec- 


NERVUS  OPTICUS. 


151 


tive-tissue.    When  the  trabeculae  become  thus  hypertrophied, 
the  nerve  fibres  and  blood-vessels  are  accordingly  compressed, 


Fig.  83.— Interstitial  inflammation  of  the  optic  nerve.     Longitudinal  section. 

and  the  thus  impaired  nutrition,  leads  to  atrophy  of  the 
nerve  fibres,  of  which  latter  we  have  two  different  forms.  In 
one  of  them  the  nerve  fibres  become  simply  thinner,  and  we 
find  lying  between  them  a  number  of  fatty  cells,  probably 
aeuroglia  cells  undergoing  a  regresssive  metamorphosis ;  in  the 


Fig.  84.— Interstitial  inflammation  of  the  optic  nerve.    Transverse  section. 

other  form  the  whole  of  the  nervous  elements  is  represented 
by  a  grumous  substance,  formed  of  molecular  fat  drops,  that 


1 5  2  THE  HUM  A  N  E  YE. 

is,  detritus.  The  connective-tissue  grows  thicker  and  thicker 
and  this  fatty  substance  or  the  simply  atrophying  nerve  fibres 
disappear  more  and  more.  The  process  as  a  rule  attacks 
some  part  of  the  optic  nerve  more  than  the  other,  and 
thus  the  periphery  of  the  nerve  or  a  sector  (in  a  transverse 
section)  may  appear  perfectly  atrophied,  while  the  remainder 
may  as  yet  be  little  altered. 

At  the  same  time  the  optic  papilla  is  filled  with  round- 
cells,  and  its  connective-tissue  also  becomes  gradually  hyper- 
trophied,  while  the  nervous  elements  become  atrophic. 
Among  the  latter  we  frequently  find  nerve  fibres  having  a 
spindle-shaped  swelling  of  varying  size,  which  has  been  called 
"  sclerotic  hypertrophy  "  of  the  nerve  fibres.  I  have  never 
been  able  to  see  nuclei  in  these  swellings.  Cells  undergo- 
ing fatty  metamorphosis  are  also  found,  and  are  probably 
cells  of  the  neuroglia. 

When  the  new-formed  connective-tissue  gradually  shrinks 
the  optic  nerve,  which  had  before  been  greatly  thickened, 
becomes  thinner,  and  its  blood-vessels,  which  are  thus  com- 
pressed become  atrophied.  The  formerly  much  swollen 
papilla  decreases  in  height  and  shows  a  gradually  deepening 
flat  excavation,  the  so-called  atrophic  excavation  of  the  optic 
papilla. 

Such  an  atrophy  of  the  optic  nerve  and  papilla  must,  of 
course,  influence  the  condition  of  the  retina.  We  find  its  nerve 
fibre  layer  always  thinner  than  normal.  In  later  stages  of  the 
affection,  perivasculitis  and  interstitial  retinitis  are  observed. 

Interstitial  neuritis  may  remain  stationary  at  any  period, 
but  it  is  generally  progressive.  Nerves  in  which  nervous 
elements  can  no  longer  be  detected,  and  which  are  totally 
changed  into  connective-tissue,  are,  however,  but  rarely  seen. 

Haemorrhages  occurring  in  the  optic  nerve  during  the 
progress  of  the  disease,  leave  their  traces  behind  in  the  shape 
of  crystals  of  haematoidine. 

The  sheaths  of  the  optic  nerve  also  generally  become  in- 
flamed and  hypertrophied. 

d.  Medullary  Neuritis. 
Although  the  possibility  of  a  primary  medullary  neuritis 


NERVUS  OPTICUS. 


153 


cannot  a  priori  be  denied,  it  is  certain  that  the  nervous  ele- 
ments are  not  prone  to  active  inflamation.  I  have  never  seen 
a  case  of  neuritis  in  which  I  thought  myself  justified  in  con- 
sidering the  nerve  fibres  as  the  seat  of  the  primary  inflamma- 
tion. The  description  of  this  form  of  neuritis  given  by  Leber 
agrees  essentially  with  mine,  of  the  changes  in  the  nerve  and 
papilla  in  cases  of  interstitial  neuritis,  but  I  cannot  consider 
it  as  evidence  of  the  existence  of  such  a  primary  medullary 
neuritis  optici. 

Results. 

Besides  the  dropsical  enlargement  of  the  intervaginal 
space  combined  with  stretching  of  the  outer  sheath  of  the 
optic  nerve,  and  its  obliteration  by  new-formed  connective- 
tissue,  the  most  important  and  frequent  results  of  the  affec- 
tions just  described,  are  atrophy  of  the  optic  nerve  and 
papilla,  and  consequent  alterations  in  the  retina. 

Even  when  the  nervous  elements  of  the  optic  nerve 
have  been  totally  destroyed,  we  find  the  connective-tissue 
arranged  in  a  manner  resembling  the  normal  condition  (at 
least  in  the  longitudinal  direction).  Such  nerves,  however, 
but  rarely  come  under  observation.  In  most  cases  we  find 
only  the  connective-tissue  trabeculae  very  considerably  thick- 
ened at  the  expense  of  the  nerve  fibres.  Their  sclerotic  ap- 
pearance is  still  more  striking  than  in  the  normal  and  the 
blood-vessels  are  greatly  reduced  in  number.  The  remaining 
nerve  fibres  have  either  lost  their  medulla,  grown  very  thin 
and  lie  as  indifferent  fibres,  which  can  be  stained  with  car- 
mine, between  the  connective-tissue  fibres,  or  they  appear 
changed  into  a  yellowish,  grumous  substance,  which  cannot 
be  stained  by  any  staining  material,  and  consists  of  drops  of 
fat  and  myeline  of  varying  size. 

Inward  from  the  hypertrophied  lamina  cribrosa,  the  con- 
nective-tissue of  the  papillae  is  also  hypertrophic,  and  the 
nervous  elements  are  destroyed  or  thin  and  atrophic.  In  the 
latter  case  they  may  still  be  distinguished  from  the  connec- 
tive-tissue. Some  nerve  fibres  may  be  found  in  a  state  of 
sclerotic  hypertrophy,  as  described  above.     In   later  stages 


154 


THE  HUMAN  EYE. 


we  find  that  the  papilla  consists  chiefly  of  a  network  of  areo- 
lar connective-tissue,  the  meshes  of  which  appear  empty. 

In  the  farther  progress  of  the  affection,  the  new-formed 
connective-tissue  shrinks,  and  from  this  shrinkage  the  so- 
called  atrophic  excavation  of  the  papilla  nervi  optici  ensues  ; 
and  the  gradually  flattened  papilla  may  finally  be  nearly  or 
entirely  reduced  to  the  lamina  cribrosa,  which  in  this  afifec- 


FiG.  85.— Atrophic  excavation  of  the  optic  papilla  filled  with  a  delicate  connective-tissue 
formed  in  the  neighboring  vitreous  body. 

tion  always  remains  in  its  normal  position.  (See  Fig,  85). 
The  walls  of  the  remaining  blood-vessels  are  thickened  and 
sclerosed.  Atrophy  of  the  optic  nerve  and  papilla  leaves  in 
its  wake  atrophy  of  the  nerve  fibre  layer  of  the  retina,  and 
regressive  metamorphosis  of  the  ganglionic  cells. 

During  the  inflammatory  affections  of  the  papilla  nervi 
optici,  the  adjacent  part  of  the  vitreous  body  also  seem  fre- 
quently to  become  inflamed.  As  a  result  of  this  inflamma- 
tion (circumscribed  plastic  hyalitis)  we  see  a  small  amount 
of  connective-tissue  formed  in  the  posterior  parts  of  the 
vitreous  body,  into  which  blood-vessels  starting  from  the 
papilla  are  seen  to  enter.  If  in  such  cases  an  atrophic  excava- 
tion of  the  papilla  is  formed,  we  may  find  the  latter  filled  with 
delicate  connective-tissue,  which  anteriorly  is  lost  in  the 
vitreous  body.  (See  Fig.  85).  The  granuloma  of  the  optic 
nerve  to  be  described  later  on,  is  not  to  be  confounded  with 
this  affection. 


NERVUS  OPTICUS. 


Appendix. 


155 


Glaucomatous  Atrophy  and  Excavation,  and  Embolic  Atrophy 
of  the  Optic  Nerve. 

In  the  foregoing,  we  have  had  occasion  several  times  to 
state  that,  in  spite  of  a  large  number  of  very  careful  inves- 
tigations, we  are  not  yet  in  the  possession  of  an  anato- 
mical explanation  of  the  cause  of  the  array  of  symptoms 
to  which  we  apply  the  clinical  name  of  glaucoma.  Knies, 
too,  who  thought  to  have  found  this  cause  in  the  obliteration 
of  Fontana's  spaces,  has  certainly  gone  beyond  the  mark, 
since,  as  many  have  already  proven,  this  obliteration  is  often 
found  without  having  caused  glaucoma,  and  on  the  other 
hand,  is  frequently  wanting  in  glaucomatous  eyes.  My  own 
investigations  concerning  a  large  number  of  glaucomatous 
eyes,  have  not  taught  me  any  anatomical  fact,  which  can 
be  considered  as  the  common  cause  of  this  disease.  Its  most 
important  symptom  is  certainly  atrophy  of  the  optic  nerve, 
and  glaucomatous  excavation  of  the  optic  papilla.  The 
anatomical  conditions  of  a  glaucomatous  excavation  are  so 
characteristic  that  they  always  enable  us  to  make  a  positive 
diagnosis. 

While  simple  atrophic  excavation  is  flat,  and  only  reaches 
to  the  lamina  cribrosa,  which,  as  stated,  remains  in  its  normal 
position,  we  find  in  a  case  of  glaucomatous  excavation  that 
the  fibres  of  the  lamina  cribrosa  are  compressed  and  forced 
backward,  often  behind  the  outer  surface  of  the  sclerotic. 
The  nerve  fibres  of  the  papilla  which  are  pressed  aside  are 
atrophied,  and  the  optic  nerve  behind  the  lamina  cribrosa 
shows  the  conditions  of  atrophy  after  interstitial  neuritis. 
(See  Fig.  86). 

Led  by  clinical  observation,  Schnabel  sought  the  cause  of 
glaucoma  in  an  inflammatory  process  of  the  tissues  surround- 
ing the  optic  nerve  entrance,  especially  of  the  choroid.  This 
idea  seemed  to  be  rather  plausible,  and  I  tried  hard  to  find 
anatomical  facts  to  prove  it.  I  could  not,  however,  find  them. 
In  most  of  the  cases  of  glaucoma,  I  had  the  opportunity  to 
examine,  I  found  the  choroid  normal ;  in  one  case  it  appeared 


156 


THE  HUMAN  E  YE. 


inflamed  on  the  nasal  side  of  the  papilla,  and  was  infiltrated 
with  round-cells ;  in  a  number  of  cases  the  choroid  was  atro- 
phied. 


Fig.  86.— Very  deep  glaucomatous  excavation.    Atrophy  of  the  optic  nerve. 

To  sum  up,  the  essential  difference  between  an  atrophic 
and  a  glaucomatous  excavation  of  the  papilla  nervi  optici,  is 
the  following,  viz.,  in  the  former  affection  the  papilla  and 
optic  nerve  are  affected,  while  the  lamina  cribrosa  retains  its 
normal  position,  in  the  latter  the  lamina  cribrosa  is  pressed 
outward,  while  atrophy  of  the  papilla  and  optic  nerve  takes 
place. 

According  to  Schweigger,  a  small  secondary  excavation 
may  be  found  in  the  larger  one,  if  in  consequence  of  the  glau- 
coma the  tissue  surrounding  the  central  retinal  blood-vessels 
is  also  distended. 

We  frequently  find  also  in  glaucomatous  excavations,  a 
delicate  connective-tissue,  which  is  formed  in  the  adjacent 
part  of  the  vitreous  body. 

Atrophy  of  the  optic  nerve  is,  moreover,  observed  after 
embolism  of  the  central  retinal  artery.  Anatomically,  it  in 
no  way  differs  from  the  atrophy  consequent  upon  glaucoma 
or  inflammatory  processes  within  the  optic  nerve  or  its  sur- 
roundings. Neither  has  atrophy  caused  by  retinal  affections 
anything  peculiar. 


Hcemorrhage  in  the  Optic  Nerve.     Hoematogeneous  Pigment. 

Haemorrhages  of  a  varying  size  are  not  rare  in  the  tissue 
of  the  optic  nerve.     They  may  be  caused  by  injuries  or  ope- 


NERVUS  OPTICUS. 


157 


rations,  or  may  occur  during  inflammatory  processes.  In 
recent  cases  we  find  the  optic  nerve  or  papilla  filled  with  red 
blood  corpuscles,  which  press  the  nerve  fibre  bundles  aside. 
These  blood-corpuscles  later  on  are  gradually  destroyed,  and 
the  amorphous  or  crystallized  hsematoidine  remains  lying 
within  the  connective-tissue  of  the  nerve.    (See  Fig.  87).     It 


Fig.  87. — From  an  atrophic  optic  nerve.     Hypertrophy  of  the  connective-tissue,  which  con- 
tains some  pigment.    The  nerve-fibres  are  broken  up  into  a  grumous  substance. 

is  very  probable,  as  Knapp  conjectured,  that  the  abnormal 
pigmentation,  sometimes  seen  with  the  ophthalmoscope  in 
the  papilla  nervi  optici,  is  caused  by  such  haemorrhages. 
Whether  haemorrhages  in  the  intervaginal  space  {Leber)  may 
cause  a  similar  ophthalmoscopic  picture,  seems  to  me 
doubtful. 

In  transverse  sections  of  such  pigmented  optic  nerves,  we 
frequently  find  that  the  nerve  fibre  bundles  surrounded  by 
pigmented  connective-tissue  are  atrophied.  This  atrophy  is 
probably  due  to  the  pressure  exerted  upon  them  by  the 
haemorrhage.  The  connective-tissue  in  which  the  pigment 
lies  embedded,  is  always  hypertrophied.     (See  Fig.  87). 

Tumors  of  the  Intra-Ocular  part  of  the  Optic  Nerve. 

Tumors  of  the  "  head  "  of  the  optic  nerve  have,  it  seems, 
never  been   observed.     The  tumors  of  the  optic  nerve  re- 


158 


THE  HUMAN  E  YE. 


ported  in  literature,  all  originated  in  the  intra-cranial  or 
intra-orbital  part  of  this  nerve,  and  do  not  here  come  under 
consideration. 

It  seems  that  a  direct  injury  to  the  optic  papilla  may  lead 
to  the  formation  of  a  granuloma ;  I  had,  at  least  once,  the 
opportunity  of  examining  such  a  tumor.  It  consisted  of 
round-cells  and  small  spindle-cells,  which  lay  between  a  fine 
network  of  connective-tissue  and  blood-vessels.  The  con- 
nective-tissue and  the  blood-vessels  of  the  tumor  were  con- 
tinuations of  those  parts  in  the  papilla  nervi  optici.  (^See 
Fig.  88). 


Fig.  88.— Granuloma  of  the  optic  papilla. 

The  similiarity  between  such  an  anatomical  condition  and 
the  one  clinically  observed  by  Manz,  and  called  retinitis 
proliferans,  and  the  affections  drawn  and  described  by  JcBger 
and  Becker  as  new-formation  of  connective-tissue  and  blood- 
vessels in  the  vitreous  body,  is  very  striking.  In  the  cases 
reported  by  these  authors,  the  eyes  however,  were,  not  in- 
jured. 


VIII. 

RETINA. 

I.  Normal  Condition. 

The  retina  consists  of  ten  distinct  layers,  if  we  count  the 
pigmented  epithelium  as  part  of  this  membrane.  We  have 
treated  of  this  layer  already,  and  considered  it  as  a  sepa- 
rate one,  in  which  I  think  we  are  the  more  justified,  since  a 
direct  proof  of  the  genetic  connection  between  the  retina  and 
the  pigmented  epithelium  has  yet  to  be  found. 

The  layers  of  the  retina  are  therefore  the  following  : 

1.  Internal  limiting  membrane. 

2.  Nerve  fibre  layer. 

3.  Ganglionic  layer. 

4.  Inner  molecular  layer. 

5.  Inner  granular  layer. 

6.  Outer  molecular  layer. 

7.  Outer  granular  layer. 

8.  External  limiting  membrane  (?) 

9.  Rods  and  cones. 

The  first  six  of  these  layers  have  by  Schwalbe  been  called 
the  brain  layer  of  the  retina,  the  remaining  three  the  neuro- 
epithelial layer. 

The  different  elements  of  the  retina  are  held  in  position 
by  a  common,  easily  distinguished  substance  (supporting- 
tissue)  which  forms  the  so-called  supporting  or  radiary  fibres 
of  the  retina.  Schwalbe  says  that  this  substance  is  not  true 
connective-tissue.  Pathological  processes,  however,  prove  it 
to  be  in  no  way  different  from  it. 

The  radiary  fibres  traverse  the  retinal  tissue  at  right 
angles  to  its  surfaces.  They  are  flat  cylindrical  structures 
having  on  their  sides  wing-like  offsets  of  varying  shape  which 
anastomose  with  each  other.  Every  radiary  fibre  has  within 
the  inner  granular  layer  an  oval  nucleus  which  is  either  en- 
closed in  a  spindle-shaped  enlargement,  or,  as  it  seems  fre- 


l6o  THE  HUMAN  EYE. 

quently,  only  adheres  to  the  fibre.  By  the  site  of  this  nucleus 
the  radiary  fibres  are  divided  into  an  inner  and  an  outer  part. 
Their  inner  part  ends  with  a  cone-like  swelling  within  the 
nerve  fibre  layer  at  the  internal  limiting  membrane.  Their 
outer  part  reaches  the  limitans  externa.  According  to 
Schwalbe,  the  cone-like  swelling  of  the  inner  part  of  the 
radiary  fibres  also  contains  a  nucleus.  I  have  never  been 
able  to  see  it. 

Merkel  states  that  the  supporting  tissue  forms  a  tube-like 
sheath  for  every  cone-fibre  and  every  cone-granule,  and  he 
draws  a  similar  sheath  around  the  rods.  In  teased  specimens 
the  former  may  without  doubt  frequently  be  seen. 

The  limitans  interna  and  externa  enclose,  so  to  speak,  the 
retina.  In  transverse  sections  the  former  always  appears  as 
a  double-contoured,  vitreous  membrane.  Recent  authors 
have  denied  the  existence  of  an  internal  limiting  membrane, 
and  stated  that,  what  appeared  to  be  such,  was  formed  by  the 
coalescence  of  the  cone-like  enlargements  of  the  inner  part 
of  the  radiary  fibres.  This  they  declare  to  be  proven,  since 
in  a  plain  view  of  the  inner  surface  of  the  retina,  we  can  see 
the  basis  of  these  cone-shaped  ends,  and  when  they  are 
stained  with  nitrate  of  silver,  their  Outlines  are  very  similar 
to  those  of  endothelial  cells.  I  am  not  prepared  to  agree  with 
these  authors,  and  must  insist  upon  the  existence  of  a  separate 
internal  limiting  membrane,  which  is  not  formed  by  the  coales- 
cence of  the  basis  of  the  cone-shaped  terminus  of  the  support- 
ing fibres,  but  which  covers  these  and  can  become  detached  by 
itself,  as  we  frequently  find  it  in  pathological  eyes.  Besides 
I  once  had  an  opportunity  to  observe  vitreous  bodies  lying 
upon  it,  similar  in  appearance  and  nature  to  those  of  the 
lamina  vitrea  of  the  choroid.  I  consider  this  to  be  a  further 
proof  of  the  existence  of  a  separate  internal  limiting  mem- 
brane, similar  to  the  lamina  vitrea  of  the  choroid,  and  the 
membrana  Descemetii.  This  membrane  is,  however,  not  to 
be  confounded  with  what  has  been  called  the  hyaloid  mem- 
brane, and  which  will  be  spoken  of  in  Chapter  X. 

While  I  thus  unite  in  the  opinion  of  those  authors  who 
acknowledge  the  existence  of  an  internal  limiting  membrane, 
I  do  not  consider  that,  what  has  been  called  the  external 


RETINA.  16 1 

limiting  membrane,  is  really  a  membrane.  In  the  outer 
granular  layer,  all  the  parts  of  the  supporting  tissue  coalesce 
in  such  a  way  that  they  fill  all  the  spaces  between  the  fibres 
of  the  rods  and  cones  and  their  granules.  The  free  ends  of 
the  rods  and  cones  reach  beyond  this, — sit  venia  verbo — 
cementing  substance,  and  the  outer  surface  of  the  latter  rep- 
resents in  transverse  sections  a  single  line,  which  is  sharply 
defined,  but  is  not  a  membrane.  If  the  latter  were  the  case, 
we  would  see  a  double  contour. 

The  sheaths  of  the  outer  parts  of  the  rods  and  cones 
reach  with  them  beyond  this  surface,  and  are,  as  Mcrkel 
states,  probably  open  towards  the  choroid. 

The  nerve  fibre  layer  of  the  retina  consists,  as  its  name 
implies,  chiefly  of  the  nerve  fibres  which  radiate  from  the 
optic  nerve,  as  soon  as  it  has  entered  the  eye-ball.  The  ma- 
jority of  fibres  continue  to  run  in  a  radiating  direction 
towards  the  periphery  of  the  retina.  Only  those  fibres  which 
go  to  the  macula  lutea  deviate  from  this  direction,  and 
are  concentrically  bent  into  arches,  by  which  arrangement 
a  larger  number  of  nerve  fibres  are  enabled  to  reach  the 
yellow  spot,  than  would  be  possible,  if  they  approached  it  in 
a  radiating  direction.  The  fibres  are  axis-cylinders  of  vary- 
ing thickness,  and  are  united  into  bundles.  Near  the  optic 
nerve  entrance  there  are  several  layers  of  such  bundles, 
which  at  a  short  distance  from  it  are  spread  into  one.  To- 
wards the  periphery  of  the  retina  the  thickness  of  the  nerve 
fibre  layer  continually  decreases,  and  the  fibres  end  at  the  so- 
called  ora  serrata  in  a  terminal  plexus  {Merkel).  Schwalbe 
described  flat  endothelial-like  cells  with  an  oval  nucleus  in 
this  layer.  They  are  neuroglia-cells,  and  can  be  easily  recog- 
nized as  such. 

The  nerve  fibres  are  said  to  branch  off  at  acute  angles 
while  on  their  way  to  the  ora  serrata,  and  to  anastomose  with 
each  other.  The  varicose  appearance  which  they  often  have, 
is  probably  a  post  mortem  symptom,  or  is  caused  by  chemical 
agents. 

Outwards  from  the  nerve  fibre  layer  lies  the  ganglionic 
cell  layer.  These  ganglionic  cells  form,  only  in  the  region  of 
the  macula  lutea,  several  layers.     They  lie  very  near  each 


l62  THE  HUMAN  EYE. 

other  in  the  neighborhood  of  the  optic  nerve  entrance,  and 
are  found  farther  apart  the  nearer  the  ora  serrata.  It  must 
be  mentioned  here  that  the  ganglionic  cell  layer  is  not  well 
defined,  and  many  of  its  cells  lie  in  the  nerve  fibre  or  in  the 
inner  molecular  layer. 

The  cells  themselves  vary  in  size.  They  are  round  or 
oval,  and  have  a  large  round  or  ellipsoid  nucleus  with  several 
nucleoli.  A  nerve  fibre  coming  from  the  opticus  enters  into 
every  such  ganglionic  cell,  and  we  see  springing  from  the 
cells  one  or  more  offsets  which  go  into  the  inner  molecular 
layer.  In  the  region  of  the  macula  lutea,  the  ganglionic  cells 
are  said  by  all  authors  to  be  oval  and  to  have  only  one  per- 
ipheral offset,  that  is,  to  be  bipolar.  The  ganglionic  cells  lie 
embedded  in  notches  on  the  wing-like  offsets  of  the  support- 
ing fibres.  Schwalbe  found  a  homogeneous,  lustrous  cement- 
ing substance  between  them.  The  offsets,  after  entering  the 
inner  molecular  layer,  give  off  numerous  branches  in  a  radia- 
ting or  oblique  direction.  According  to  Mcrkel,  these  branches 
then  enter  the  inner  granular-layer  and  anastomose  with  the 
central  fibres  of  the  inner  granules. 

The  inner  molecular  layer  consists  of  these  fine  fibres 
just  mentioned,  and  the  so-called  granular  (molecular)  sub- 
stance. Merkel  and  others  describe  the  latter  as  a  homo- 
geneous substance  containing  numerous  small  cavities.  These 
cavities  are  said  to  be  filled  with  fluid  which  refracts  the  light 
in  a  different  manner,  or  to  contain  solid  granules.  {^Merkel, 
Henle,  Retzius).  The  inner  molecular  layer  is  comparatively 
thick,  and  remains  of  about  the  same  thickness  all  over  the 
retina,  except  in  the  region  of  the  macula  lutea.  The  sup- 
porting fibres  simply  pass  through  it.  Retzius  states  that 
the  offsets  from  the  ganglionic  cells  have  a  radiating  direc- 
tion in  this  layer,  others  found  them  to  branch  off  at  right  or 
acute  angles  before  entering  the  inner  granular  layer. 

The  inner  granular  layer  is  mainly  formed  of  nuclei. 
We  stated  above  that  the  supporting  fibres  have  a  nucleus  in 
this  layer,  and  besides  these  we  find  another  kind  of  delicate 
oval  nuclei  with  a  nucleolus,  and  surrounded  by  a  small 
amount  of  protoplasm.  These  have  a  central  and  a  periphe- 
ral (inner  and  outer)  offset,  the  former  of  which  is  thinner 


RETINA. 


163 


than  the  latter.  According  to  Merkel  and  others,  the  central 
offsets  of  these  nuclei  of  the  inner  granular  layer,  anastomose 
with  the  peripheral  offsets  of  the  ganglionic  cells  in  the  inner 
molecular  layer.  Their  peripheral  offsets  pass  through  the 
outer  molecular  layer  in  a  radiating  direction  or  are  bent  like 
a  bayonet,  and  give  off  several  smaller  branches.  Merkel 
undoubtedly  found  an  anastomosis  between  these  peripheral 
offsets  of  the  nuclei  of  the  inner  granular  layer  and  the  central 
fibres  of  the  cones  in  the  outer  molecular  layer.  Such  an 
anastomosis  with  the  rod-fibres,  although  it  is  very  probable, 
has  as  yet  not  been  found. 

The  outer  molecular  layer  is  very  thin.  Besides  the 
fibres  just  mentioned,  we  find  in  it  a  small  quantity  of  the 
same  granular  (molecular)  substance,  with  which  we  already 
met  in  the  inner  molecular  layer.  I  can  confirm  the  statement 
oi  Merkel,  that  in  transverse  sections  of  this  layer,  nearly  with- 
out exception,  we  see  a  broken  line  (Huelfslinie).  This  is 
formed  by  the  broader  end  of  the  central  fibres  of  the  cones 
and  their  sheaths,  and  will  be  spoken  of  again  later  on. 
Schwalbe  also  found  flat  cells  in  the  outer  molecular  layer, 
the  offsets  of  which  took  part  in  the  formation  of  the  network 
of  fibres  of  which  this  layer  partly  consists.  These  cells  are 
said  to  be  of  a  ganglionic  nature. 

Rods  and  cones  and  the  outer  granular  layer,  are  accord- 
ing to  Schwalbe  the  "  neuro-epithelium  "  of  the  retina. 

Let  us  first  examine  the  cones.  The  cone-fibre  originates 
with  a  cone-shaped  swelling  in  the  outer  molecular  layer,  and 
is  there,  as  proven  by  Merkel,  in  direct  connection  with  the 
fibres  coming  from  the  inner  granular  layer.  The  cone-fibre 
then  becomes  a  little  thinner,  until  just  under  the  limitans 
externa,  it  again  swells  rapidly,  and  there  forms  the  cone 
itself.  This  part  of  the  cone,  inwards  from  the  limitans  ex- 
terna, contains  a  large  oval  nucleus  with  a  nucleolus  (the  so- 
called  cone-granule).  Besides  these  cone-fibres,  the  rod-fibres 
originate  in  the  outer  molecular  layer.  A  direct  connection 
between  the  rod-fibre  and  the  fibres  coming  from  the  inner 
granular  layer  has,  as  stated  above,  not  yet  been  found.  As 
soon  as  the  rod-fibre  has  left  the  outer  molecular  layer,  it  has 
a  small  swelling,  and  somewhat  farther  on,  near  the  limitans 


164 


THE  HUMAN  E  YE. 


externa,  it  encloses  in  a  larger  swelling  the  "  rod-granule." 
This  swelling  has  in  fresh  specimens  a  peculiar  transverse 
striation,  which  disappears  soon  after  death.  Only  then  the 
nucleus  is  distinctly  recognizable.  While  the  cone-granule 
always  lies  (except  in  the  region  of  the  macula  lutea  and  the 
ora  serrata)  just  inwards  from  the  limitans  interna,  the  rod- 
granules  which  are  much  more  numerous,  form  several  layers, 
that  is,  their  distance  from  the  limitans  externa  is  varying. 
We  find  therefore  the  rod-fibres  generally  thinner  again  to 
the  outside  of  the  swelling  which  encloses  the  granule,  until 
they  pass  over  into  the  rods  themselves. 

The  rods  and  cones  lie  outwards  from  the  limitans  externa, 
as  we  stated  before.  The  cones  are  bottle-shaped  structures 
which  spring  from  the  part  of  the  cone-fibre  containing  the 
nucleus ;  they  consist  of  the  inner  conical  and  the  outer 
thinner  cylindrical  part.  The  inner  part  appears  granulated, 
and  encloses  in  its  outer  half,  the  so-called  ellipsoid  body,  a 
structure  the  nature  of  which  is  as  yet  not  understood.  The 
outer  part  of  the  cones  consist  of  a  homogeneous  substance 
which  refracts  the  light  strongly,  and  cannot  be  stained  with 
carmine.  After  death,  or  under  the  influence  of  several 
chemical  agents,  it  splits  into  fine  lamellae. 

The  rods,  too,  may  be  divided  into  an  inner  and  an  outer 
part.  The  inner  part  is  generally  thicker  than  the  outer,  and 
both  are,  as  a  rule,  cylindrical.  The  inner  part,  moreover, 
appears  granulated.  Their  outer  part,  too,  is  broken  up 
into  fine  lamellae  when  dying  or  under  the  influence  of  chemi- 
cal agents.  Some  authors  describe  it  as  having  a  number  of 
longitudinal  stripes  on  its  surface. 

As  stated  above,  the  rods  and  cones  with  their  fibres  and 
granules,  have  a  sheath  {Merket).  The  sheaths  of  the  cone- 
fibres  end  in  the  outer  molecular  layer,  and  their  bases  there 
form  the  broken  line,  above  referred  to.  The  longitudinal 
stripes  often  seen  on  the  surface  of  the  inner  parts  of  the  rods 
and  cones,  is  explained  by  folds  in  these  sheaths.  According 
to  Kraiise  and  Schultze,  small  fibrillae  start  from  the  limitans 
externa,  and  surround  the  basis  of  the  inner  parts  of  the  rods 
and  cones,  forming  the  so-called  fibre-baskets  (Faserkoerbe). 

In  plain  views  of  the  external  surface  of  the  retina,  the 


RETINA 


■i6s 


optical  transverse  sections  of  the  rods  and  cones,  form  a  regu- 
lar mosaic.  This  shows,  however,  a  different  arrangement 
according  to  the  region  from  which  the  specimen  is  taken. 
While  in  the  region  of  the  macula  lutea  every  cone  appears 
to  be  surrounded  by  a  single  ring  of  rods,  the  latter  are  more 
and  more  numerous  and  the  cones  farther  apart  from  each 
other,  the  nearer  they  approach  the  periphery  of  the  retina. 

Kuehne,  Boll  ^.nA  others  have  recently  found  that  during 
life  the  outer  part  of  the  rods  has  a  purple  hue,  being  satura- 
ted with  the  so-called  retinal  purple  which  is  secreted  from 
the  pigmented  epithelial  layer. 

From  the  description  given  in  the  foregoing,  the  way 
in  which  the  connection  between  the  optic  nerve  and 
the  rods  and  cones  is  established,  is  the  following:  The  opti- 
cus fibres  enter  the  ganglionic  cells  which  send  one  or  two 
peripheral  offsets  into  the  inner  molecular  layer,  where  they 
anastomose  with  the  central  offsets  of  the  nuclei  of  the  inner 
granular  layer.  The  peripheral  offsets  of  these  enter  the 
outer  molecular  layer  from  which  the  central  offsets  of  the 
rods  and  cones  (the  rod-fibres  and  cone-fibres)  are  seen  to 
emerge.  As  Merkel  has  proven,  the  peripheral  fibres  of  the 
inner  granules  are  in  direct  connection  with  the  central  off- 
sets of  the  cone-granules ;  the  same  has  not  yet  been  proven 
for  the  rods.  We  know  therefore  of  a  direct  communication 
between  the  cones  and  the  central  organ,  while  the  same  is 
not  yet  established  for  the  rods. 

It  is  certainly  a  very  remarkable  fact,  that  the  so-called 
"  visual  purple  "  which  by  recent  investigations  has  been  ac- 
corded so  important  an  influence  in  the  act  of  vision,  does 
not  tint  the  cones,  which  are  undoubtedly  percipient  organs, 
but  renders  the  rods,  which  appear  to  be  at  least  less  im- 
portant for  direct  vision,  purple.  It  would  therefore  appear 
that  the  physiological  value  of  the  visual  purple  has  been 
overrated. 

The  structure  of  the  retina,  as  we  have  described  it,  is 
very  materially  altered  in  its  peripheral  parts,  and  in  the 
region  of  the  macula  lutea. 

Near  the  ora  serrata  the  nerve  fibres,  rods  and  cones 
gradually  disappear,  while   the  supporting   tissue   becomes 


1 66 


THE  HUMAN  EYE. 


more  and  more  prevalent.  The  rapid  attenuation  observed 
in  the  periphery  of  the  retina  is,  however,  due  in  a  great 
measure  to  the  abrupt,  not  gradual  disappearance  of  the  inner 
molecular  layer.  The  granular  layers  become  gradually  thin- 
ner, and  the  outer  one  sooner  so  than  the  inner,  and  finally 
the  one  cell  layer  of  the  retina,  which  lies  upon  the  ciliary 
body  is  formed.  In  the  parts  nearest  to  the  ora  serrata,  we 
sometimes  find  (especially  in  the  eyes  of  old  people)  an  alter- 
ation which  Iwanoff  called,  as  it  seems  to  me  very  inap- 
propriately, "  oedema  "  of  the  retina.  In  plain  views  of  such 
a  retina,  when  stained,  we  see  an  irregular  network  of  light 
bands,  varying  in  breadth,  and  surrounding  islets  of  a  darker 
tint.  In  transverse  sections  we  see,  that  these  lighter  bands 
are  caused  by  a  system  of  cavities  varying  in  size,  which  lie 
in  the  inner  and  outer  granular  layer.  These  cavities  are 
round  or  oval,  and  coalesce  with  each  other,  or  are  separated 
by  pillars,  the  capitals  of  which  form  the  darker  islets  above 
referred  to  and  seen  in  the  plain  views.  These  pillars  consist 
of  fibres  with  a  nucleus  and  long  spindle-shaped  cells.  Some- 
times their  transverse  septa  are  formed  by  trabeculae  running 
in  a  transverse  direction  from  one  pillar  to  another.  Proba, 
bly  these  cavities  are  filled  with  a  serous  fluid  during  life. 
(See  Fig.  89).     This  condition  of  the  retina  I  never  found 


Fig.  89.— Cystoid  degeneration  of  the  retina  near  the  ora  serrata. 

combined  with  the  symptoms  of  retinal  oedema,  which  are 
to  be  detailed  farther  on,  and  I  therefore  think  it  much  more 
appropriate  to  call  this  condition  cystoid  degeneration  of  the 
ora  serrata  retinae  {Nettleshif). 

The  greatest  changes  in   the  structure  of  the  retina  are 


RETINA. 


167 


found  in  the  region  of  the  macula  lutea,  and  in  the  fovea 
centralis.  The  macula  lutea  according  to  Koelliker  lies,  from 
forty-two  to  forty-five  mm.  distant  from  the  optic  nerve 
entrance,  and  has  a  small  depression  somewhat  eccentrically 
situated,  viz.,  the  fovea  centralis.  The  examinations  as  to 
the  cause  of  the  yellow  tint  of  this  part  of  the  retina  are  not 
yet  concluded.  The  macula  lutea  usually  forms  an  oval,  the 
longitudinal  axis  of  which  lies  in  a  horizontal  direction. 

In  the  fovea  centralis,  the  limitans  interna  forms  a  line 
which  is  convex  towards  the  choroid.  While  the  whole  of 
the  retina  must  therefore  be  thinner  in  this  place,  its  layers 
(except  the  nerve  fibre  layer)  are  considerably  thickened  in 
the  parts  surrounding  the  fovea  centralis.  All  of  the  layers, 
however,  are  not  of  equal  thickness,  and  the  nerve  fibre 
layer  becomes  gradually  thinner,  so  much  so  that  we  find  the 
ganglionic  cells  near  the  fovea  centralis  lying  directly  under 
the  limitans  interna.  The  ganglionic  cell  layer  is  here  found 
to  be  six  or  eight  times  thicker,  than  in  other  parts  of  the 
retina,  and  its  cells  in  this  region  are  said  always  to  be  of  an 
oval  shape  and  bipolar. 

The  inner  granular  and  inner  molecular  layer  are  compara- 
tively but  little  thickened.  The  molecular  substance  of  the 
outer  molecular  layer  is  totally  wanting  in  the  fovea  centralis. 
Its  fibres  are,  however,  strongly  developed,  and  while  in  other 
parts  of  the  retina  they  run  mainly  in  a  vertical  direction, 
they  are  here  all  bent  like  a  bayonet,  so,  that  the  horizontal 
part  is  longer  than  the  others,  and  grows  more  so  the  nearer 
the  fovea  centralis.  The  outer  granular  layer  in  this  re- 
gion is  also  somewhat  thinner.  The  rods  are  as  already 
stated,  very  much  less  numerous,  and  the  number  of  the 
cones  is  considerably  increased,  the  latter  are  thinner  and 
considerably  longer,  than  in  other  regions  of  the  retina. 
Right  in  the  fovea  centralis  all  the  layers  of  the  retina  are  so 
close  to  each  other  and  so  much  thinner,  that  it  is  very  diffi- 
cult to  distinguish  them  from  each  other.  It  seems,  however, 
that  none  of  the  cellular  layers  disappear  entirely.  The 
supporting  fibres  are  very  much  thinner  in  the  region  of  the 
mucula  lutea,  and  in  the  fovea  centralis  itself,  they  are  alto- 
gether wanting.     The    fovea  centralis  has,  furthermore,  no 


1 68  THE  HUM  A  N  E  YE. 

rods.  Schzvalbe  states  that  the  basis  of  the  cells  of  the  pig- 
mented epithelial  layer  is  much  smaller  in  this  region,  but 
that  they  are  much  higher. 

At  the  papilla  the  retina  (except  its  nerve  fibre  layer)  ter- 
minates, as  Schwalbe  first  stated,  on  the  lateral  side  in  a 
vertical  line  ;  on  the  opposite  side  the  end  forms  an  oblique 
line,  and  the  outer  layers  reach  farther  towards  the  optic 
nerve  than  the  inner  ones.  The  rod-fibres  and  cone-fibres 
must  therefore  also  here,  as  in  the  region  of  the  macula  lutea, 
run  in  an  oblique  direction, 

2.  Pathological  Conditions. 

A.  CEdema  Retince. 

OEdema  of  the  retina  may  be  a  purely  passive  infiltra- 
tion of  this  membrane  with  serous  fluid  caused  by  an  affec- 
tion of  the  choroid,  or  it  may  be  more  or  less  the  result  of 
an  inflammatory  process  in  the  retina  itself. 

In  the  latter  case,  the  affection  is  always  accompanied  by 
hypersemia  of  the  retinal  blood-vessels,  while  in  the  former, 
hyperaemiais  usually  wanting.  In  oedema  of  the  retina  we  find 
all  the  elements  constituting  this  membrane  saturated  with 
a  serous  fluid.  They  consequently  appear  swollen  and  some- 
what dim.  Moreover,  there  are  a  small  quantity  of  lymph- 
cells  to  be  seen  in  the  nerve  fibre  layer.  In  consequence  of 
these  changes,  the  whole  of  the  retina  is  thicker  than  normal, 
which  is,  however,  most  pronounced  in  the  neighborhood 
of  the  optic  papilla.  Later  on  small  cavities  filled  with  serum 
may  be  found  in  the  connective  supporting  tissue  and  in  the 
molecular  substance,  especially  in  the  outer  molecular  layer. 
These  press  the  cellular  elements  aside,  and  the  latter  may 
at  a  remote  period  be  destroyed  in  consequence  of  fatty  de- 
generation, resulting  from  the  undue  pressure  exerted  upon 
them.  In  this  way  the  cavities  may  grow  larger,  and  the 
serum  which  fills  them  wjll  then  contain  some  detritus  besides 
the  lymph-cells.  The  cavities  have  mostly  an  oval  shape. 
Capillary  haemorrhages  are  but  rarely  observed  in  the  course 
of  such  an  oedema. 

CEdema  may  be  found  in  all  parts  of  the  retina,  and  is 


RETINA.  i6q 

not,  like  the  cystoid  degeneration  of  the  parts  near  the  ora 
serrata,  confined  to  one  region.  In  the  latter  affection, 
moreover,  the  hyperaemia  of  the  blood-vessels  and  the  serous 
imbibition  of  the  cellular  elements  which  surround  the  cavi- 
ties, are  wanting. 

A  number  of  larger  serous  cysts  have  been  described  in 
detached  retina.  Whether  they  have  originated  in  such  an 
oedema,  I  cannot  tell. 

I  have  not  been  able  to  ascertain  what  the  final  changes 
in  retinal  oedema  are  ;  but  it  seems  that  it  may  exist  as  a 
chronic  affection  for  a  very  long  time,  without  changing 
the  retinal  tissue  in  any  other  way  than  in  the  manner  above 
described. 

B.  Inflammatory  Processes  in  the  Retina,  and  their  Results. 

Retinitis  like  choroiditis,  has  been  clinically  divided  into 
a  large  number  of  varieties.  The  histological  conditions  do 
not  however  warrant  these  clinical  distinctions.  The  nervous 
elements  of  the  retina,  like  those  of  the  opticus,  are  not  apt  to 
become  independently  inflamed.  The  inflammatory  process 
seems  always  to  originate  in  the  connective-tissue  of  the 
retina,  and  its  nervous  elements  become  only  secondarily 
affected.  We  will  speak,  i.  of  retinitis  as  we  find  it  as  a  pecu- 
liar symptom  in  albuminuria,  2.  of  diffuse  atrophic  retinitis, 
and  3.  of  purulent  retinitis. 

a.  Retinitis  Albuminurica. 

The  peculiar  form  of  interstitial  retinitis  found  especially 
during  an  inflammatory  process  in  the  kidneys,  concerns  pre- 
eminently those  regions  of  the  retina  in  the  neighborhood  of 
the  optic  papilla  and  the  macula  lutea.  Within  these  regions 
all  the  parts  of  the  retina  gradually  suffer  from  the  affection 
and  in  advanced  cases  we  find  not  only  the  blood-vessels  and 
connective-tissue,  but  also  the  nerve  elements  (these  only 
secondarily)  altered. 

The  most  visible,  microscopical  symptom  of  this  affection 
is  the  considerable  swelling  of  the  involved  parts,  especially 
of  the  optic  papilla  and  its  surroundings.  Furthermore,  the 
thickened  retina  around  the  optic  papilla  is  usually  wrinkled 


I/O 


THE  HUMAN  E  YE. 


and  partially  detached.  The  considerable  swelling  is  chiefly 
due  to  an  inflammatory  infiltration  and  hyperplasia  of  the 
connective-tissue  and  oedema.  The  connective-tissue  fibres 
are  longer  and  thicker,  and  have  that  sclerotic  appearance 
caused  by  a  strong  refraction  of  the  light,  which  we  found 
to  be  normal  to  the  fibres  of  the  ligamentum  pectinatum. 
The  hyperplasia  and  swelling  are  most  pronounced  in  the 
nerve  fibre-layer,  especially  in  the  papilla.  The  hyper- 
semic  blood-vessels  are  usually  surrounded  by  white  blood- 
corpuscles,  which  lie  in  the  neighboring  connective-tissue. 
The  fluid  with  which  all  elements  of  the  nerve  fibre  layer 
seem  to  be  sodden,  is  homogenous,  in  some  cases  it  appears 
somewhat  granular.  The  swelling  of  the  nerve  fibre  layer  is, 
furthermore,  due  to  the  peculiar  club-like  swelling  of  the 
nerve  fibres,  already  above  described,  as  sclerotic  atrophy  of 
these  elements.  We  not  unfrequently  see  such  nerve  fibres 
in  teased  specimens.  They  are  either  thickened  at  one  or 
both  ends  or  altogether,  and  refract  the  light  strongly.  The 
thickened  part  is  very  darkly  tinted  when  carmine  has  been 
used.  As  stated  already,  I  have  never  found  nuclei  in  these 
swellings.  Nerve-fibres  which  have  been  altered  in  such 
a  way  are  not  only  found  lying  indiscriminately  among  the 
others,  but  sometimes  they  are  seen  crowded  together  in 
larger  quantities.  Where  this  is  the  case,  the  nerve  fibre 
layer  appears  to  be  more  especially  swollen,  it  projects  more 
or  less  into  the  vitreous  body  above  the  surrounding  parts, 
and  crowds  the  outer  layers  of  the  retina  close  together.  (See 
Fig.  90).  Former  authors  have  also  mentioned  a  sclerotic 
swelling  of  the  ganglionic  cells,  which  by  more  recent  authors 
is  declared  to  be  erroneous.  I  must,  however,  state  again 
that  besides  the  sclerotic  swelling  of  the  nerve  fibres,  which 
as  I  said  contain  no  nucleus,  I  frequently  found  large  round 
and  sometimes  star-shaped  bodies,  undoubtedly  containing 
a  nucleus,  and  which  I  consider  to  be  such  sclerosed  gang- 
lionic cells. 

We  find,  furthermore,  in  the  nerve  fibre  layer,  and  espe- 
cially in  the  region  of  the  macula  lutea,  cells  which  contain 
numerous  fat-granules.  They  appear  round  or  semi-lunar, 
have  one  or  more  offsets,  and  a  shining  round   nucleus.     I 


RETINA.  Y-ji 

think,  these  cells,  too,  may  be  considered  as  ganglionic  ones 
undergoing    a    regressive    metamorphosis.     I    must     state, 


Fig.  90. — Albuminuric  retinitis,     i.  Nerve  fibre   layer,  considerably    thickened    through 
sclerosed  hypertrophic  nerve  fibres.    2.  Haemorrhage. 

however,  that  the  majority  of  the  ganglionic  cells  appear  un- 
altered, so  does  the  inner  molecular  layer. 

Besides  the  round-cells  which  lie  around  the  blood-vessels 
and  those  scattered  among  the  elements  of  the  nerve  fibre 
layer,  I  not  unfrequently  found  tubercle-like  aggregations  of 
round-cells  in  this  layer. 

The  swelling  of  the  nerve  fibre  layer  may,  moreover,  be 
increased  by  a  granular  exudation,  found  under  the  limitans 
interna.  This  exudation  sometimes  detaches  the  inner  limi- 
ting membrane  to  some  extent,  and  thus  makes  it  protrude 
into  the  vitreous  body. 

Further  changes  characteristic  of  albuminuric  retinitis, 
are  found  in  the  outer  layers  of  the  retina.  In  these,  also, 
we  find  the  connective-tissue  in  a  state  of  hypertrophy 
and  partly  sclerosed,  or  in  a  state  of  fatty  infiltration.  A 
more  striking  change  is,  however,  the  formation  of  cavities 
in  the  inner  and  outer  granular,  and  in  the  outer  mole- 
cular layer.  These  cavities  are  round  or  oval,  and  in  the 
latter  case,  their  longitudinal  diameter  usually  lies  at  right 
angles  to  the  surface  of  the  retina.  The  cavities  found  in 
the  region  of  the  macula  lutea  generally  make  an  exception 
to  this  rule,  and  lie  parallel  with  the  surface  of  the  retina. 
If  the  cavities  are  small,  they  lie  either  in  one  of  the  three 
named  layers  or  in  two  neighboring  ones  (the  inner  granular 
and  outer  molecular,  or  the  latter  and  outer  granular  layers). 
The  larger  cavities  may  reach  from  the  inner  granular  layer 


172 


THE  HUMAN  E  YE. 


even  to  the  rods  and  cones.  We  found  similiar  cavities  in 
cases  of  oedema  of  the  retina.  While  these,  however,  are 
filled  with  a  serous  fluid,  the  cavities  found  in  albuminuric 
retinitis  contain  threads  of  fibrine  or  cellular  elements.  (See 
91).  The  latter  are  large  round  cells,  filled  with  fat- 
3  4 


Fig 


Fig.  Qi. — Albtcinniicric  retinitis.  1.  Outer  granular  layer.  2.  Inner  granular  layer.  3. 
Cavity  filled  with  fibrine.  4.  Cavity  tilled  with  cells  containing  fat-granules.  Both 
cavities  containing,  moreover,  peculiar  structures  of  varying  size,  which  coalesce  and 
refract  the  light  very  strongly.     Some  fat  granule  cells  lie  in  the  outer  granular  layer. 

granules  and  they  have  a  small  shining  round  nucleus,  often 
one  or  more  offsets,  and  are  of  slightly  brownish  tint.  Be- 
tween these  cells  drop-like  yellow-brown  bodies  frequently 
lie,  varying  in  size,  which  may  be  seen  to  coalesce.  The 
hardening  fluids  seem  to  cause  a  shrinking  of  these  bodies, 
and  their  surface  consequently  may  appear  wrinkled.  Some 
of  them  have  a  notch,  into  which  one  of  the  fatty  cells  would 
fit.  The  substance  which  forms  these  bodies  is  too  darkly 
tinted,  and  too  hard  to  be  considered  beyond  doubt  as  a  col- 
loid substance,  it  appears  to  be  more  like  amyloid  substance. 
It  lacks,  however,  the  concentric  structure,  and  with  iodine 
does  not  show  the  reaction  so  characteristic  of  the  amyloid 
substance.  Perhaps,  these  bodies  are  the  result  of  a  further 
regressive  metamorphosis  of  the  above-named  cells  filled  with 
fat-granules,  or  they  may  be  simply  an  exudation  coagulated 
under  the  influence  of  the  hardening  fluid. 

The  fibrine  seen  in  such  cavities  always  forms  a  net- 
work of  fine  threads,  similar  to  those  found  in  the  alveoli 
of  the  lungs  in  croupous  pneumonia.  Cells  and  fibrine 
are  but   rarely  found  together  in    the  same  cavity.     These 


RETINA. 


"^71 


cavities  contain  either  cells  or  fibrine  and  seem  never  to  be 
empty. 

A  fibrinous  exudation  frequently  lies  between  the  retina 
and  the  pigmented  epithelial  layer,  and  this  seems  to  be  found 
most  frequently  in  the  region  of  the  macula  lutea.  Where- 
cver  it  is  found,  the  rods  and  cones  are  changed  into  short 
club-shaped  structures.  This  change  in  the  shape  of  the 
rods  and  cones  is,  however,  not  at  all  characteristic  of  albu- 
minuric retinitis.  These  sometimes  may  be  altered  in 
another  manner  which  I  never  met  with  in  other  diseases  of 
the  retina.  I  am  in  the  possession  of  specimens  where  the 
rods  and  cones  in  the  neighborhood  of  the  papilla,  are  two 
and  three  times  longer  than  in  the  normal  state.  Such 
elongated  (hypertrophied)  rods  and  cones  are  somewhat 
granular,  and  in  appearance  are  similar  to  the  sclerosed  nerve 
fibres  and  ganglionic  cells,  that  is,  they  refract  the  light  very 
strongly  and  are  stained  very  dark  with  carmine.  It  is, 
furthermore,  impossible  to  distinguish  between  their  outer 
and  inner  part,  and  they  are  firmly  adherent  to  each  other. 

The  rods  and  cones  may  also  be  broken  up  into  fine 
lamellae  and  myeline-like  drops. 

Cells  containing  fat-granules,  like  those  in  the  cavities,  are 
also  seen  scattered  about  in  the  granular  layers. 

The  blood-vessels  show  pathological  changes  which,  how- 
ever, are  not  characteristic  of  albuminuric  retinitis.  We 
hardly  ever  examine  a  retina  suffering  from  the  affection 
under  consideration,  without  finding  in  it  a  large  number  of 
haemorrhages.  These  are  either  found  only  in  the  nerve  fibre 
layer  and  in  the  neighborhood  of  blood-vessels,  or  they  reach 
through  the  whole  thickness  of  the  retina  to  the  limitans  ex- 
terna, or  they  may  even  perforate  the  outer  or  inner  surface 
of  the  retina.  Crowded  red  blood-corpuscles  are  seen  between 
the  elements  of  the  retina  in  all  stages  of  destruction.  They 
usually  undergo  fatty  degeneration  before  being  absorbed. 
[Virchotv).  It  is  a  strange  fact  that  we  never  find  either 
crystals  of  haematoidine  or  any  abnormal  pigmentation  after 
such  haemorrhages  in  a  retina  suffering  from  albuminuric 
retinitis. 

These  haemorrhages    are    undoubtedly    caused   by   some 


174 


THE  HUMAN  EYE. 


pathological  changes  in  the  walls  of  the  blood-vessels  and 
cannot  be  explained  by  the  simple  process  of  diapedesis. 
The  existence  of  such  changes  is,  however,  very  difficult  to 
prove.  I  have  sometimes  found  a  fatty  infiltration  of  the 
endothelial  cells  of  blood-vessels.  Other  changes,  found  in 
the  walls  of  the  blood-vessels  can  hardly  be  the  cause  of 
these  haemorrhages,  as  they  are  found  in  other  diseases  with- 
out causing  them.  I  mean  the  sclerosis  of  the  blood-vessels 
and  a  slight  degree  of  perivasculitis.  The  characteristic  fea- 
tures of  sclerosis  of  the  blood-vessels  are,  that  their  walls  be- 
come very  thick,  (and  the  lumen  consequently  very  narrow), 
appear  hyaline  and  refract  the  light  strongly.  Sometimes 
the  thickening  of  the  walls  leads  to  perfect  obliteration  of  the 
blood-vessels.  This  process,  which  seems  to  chiefly  attack 
the  smaller  branches,  may,  moreover,  cause  the  formation  of 
a  thrombus  in  the  blood-vessels. 

In  cases  of  perivasculitis,  we  find  the  adventitia  of  the 
blood-vessels  filled  with  round-cells.  This  affection  is,  how- 
ever, of  rare  occurrence  in  albuminuric  retinitis. 

During  this  disease  of  the  retina,  the  optic  nerve  often 
shows  the  symptoms  of  interstitial  neuritis. 

b.  Retinitis  Inter stitialis  Diffusa  {Atrophica). 

Diffuse  interstitial  retinitis  is  very  frequently  observed  in 
phthisical  eye-balls.  It  is,  moreover,  caused  by  compound 
injuries  to  the  eye,  which  do  not  lead  to  phthisis,  and  by  such 
injuries  as  are  inflicted  directly  upon  the  retina  itself.  De- 
tached retinae  also  usually  show  the  symptoms  of  this  variety 
of  retinitis,  especially  when  the  folds  of  the  detached  retina 
are  glued  together  into  one  cord.  In  the  so-called  pigmenta- 
ry retinitis,  diffuse  interstitial  retinitis  is  only  a  secondary 
symptom. 

The  cases  which  so  far  have  been  submitted  to  anatomi- 
cal examination,  it  seems  all  showed  the  disease  in  a  too  far 
advanced  stage,  to  allow  of  determining  the  original  seat  of 
this  affection.  Diffuse  interstitial  retinitis,  unlike  albuminu- 
ric retinitis,  is  not  confined  to  certain  regions  of  the  retina, 
except  in  staphylomatous  and  glaucomatous  eyes.  In  the 
former  the  process  is  confined  to  the   staphylomatous  por- 


RETINA. 


175 


tions,  in  the  latter  (at  least  at  the  beginning  of  the  disease)  to 
the  neighborhood  of  the  optic  papilla. 

In  whatever  region  of  the  retina  the  affection  begins,  it 
always  attacks  at  first  the  inner  layers  of  this  membrane  and, 
even  where  the  disease  is  far  advanced,  the  outer  layers  may 
yet  be  found  in  a  comparatively  normal  condition.  The  rods 
and  cones  make  an  exception  to  this  rule,  especially  in  cases 
of  detachment  of  the  retina. 

According  to  Leber,  we  find  in  the  first  stage  of  the  affec- 
tion under  consideration,  the  nerve  fibre  layer  thickened  in 
consequence  of  a  round-cell  infiltration  which  is  most  pro- 
nounced along  the  blood-vessels.  This  cell-infiltration  leads 
to  the  new-formation  of  connective-tissue  in  the  nerve  fibre 
layer  and  the  ganglionic  cell  layer.  We  find  accordingly  at 
this  period  in  transverse  sections,  connective-tissue  hyper- 
trophy, some  of  the  nerve  fibres  and  ganglionic  cells  under- 
going a  regressive  metamorphosis,  and  the  remainder  of  them 
crowded  aside  by  the  connective-tissue.  Soon  also  the  sup- 
porting (radiating)  fibres  become  thicker,  and  they  frequently 
assume  the  sclerosed  appearance  above  referred  to.  The  ad- 
ventitia  of  the  blood-vessels,  which  in  the  beginning  appears 
infiltrated  with  round-cells,  is  also  thickened  by  the  transfor- 
mation of  these  cells  into  connective-tissue  and  the  lumen  of 
the  blood-vessels  is  accordingly  narrow. 

When  the  new-formed  connective-tissue  begins  to  shrink, 
the  nerve  fibres  and  ganglionic  cells  gradually  disappear 
through  fatty  degeneration.  Sometimes  we  also  find  gang- 
lionic cells  undergoing  a  colloid  metamorphosis.  In  conse- 
quence of  these  changes,  the  nerve  fibre  layer  (and  by  this 
means  the  whole  of  the  retina)  becomes  very  much  thinner. 

The  hypertrophy  of  the  radiating  fibres  is  sometimes  so 
considerable,  that  they  perforate  the  internal  limiting  mem- 
brane, and  form  little  connective-tissue  tumors  on  its  inner 
surface,  which  may  either  be  flat  and  have  a  broad  basis,  or 
have  a  thin  pedicle.  Moreover,  this  form  of  retinitis  is  very 
frequently  combined  with  the  new-formation  of  connective- 
tissue  in  the  peripheral  layers  of  the  vitreous  body  (those 
touching  the  inner  surface  of.  the  retina).  This  new-formed 
connective-tissue,  which  always  firmly  adheres  to  the  retina, 


i;r6  THE  HUMAN  E  YE. 

has  generally  a  lamellar  structure,  and  is  often  thicker  than 
the  retina  itself.  In  other  cases  we  find  the  connective-tissue 
of  the  nerve  fibre  layer  arranged  in  an  arcade-like  manner, 
enclosing  smaller  and  larger  spaces  and  canals,  which  are 
usually  empty  or  sometimes  contain  a  few  remains  of  the 
nerve  fibres.  These  spaces  during  life  are  probably  filled  with 
serum.  The  arcade-like  arrangement  of  the  connective-tis- 
sue seems  to  be  most  frequent  in  the  neighborhood  of  the 
optic  papilla. 

While  the  nerve  fibre  layer  undergoes  the  changes  above 
detailed,  usually  the  outer  layers  too,  begin  to  suffer,  although 
in  rare  cases,  as  stated,  they  may  reimain  intact  for  a  much 
longer  period.  The  inner  and  outer  molecular  layers  disap- 
pear at  first,  and  the  two  granular  layers  are  thus  united  into 
one.  Later  on  also,  the  cells  of  these  two  layers  can  no 
longer  resist  the  pressure  exerted  upon  them  by  the  retrac- 
tion of  the  new-formed  connective-tissue.  They  become 
granular  and  undergo  fatty  degeneration,  and  soon  the  retina 
consists  of  almost  nothing  but  connective-tissue  and  blood- 
vessels, the  walls  of  which  are  often  enormously  thickened. 
The  arrangement  of  the  connective-tissue  may,  however, 
for  a  long  time  still  imitate  the  normal  structure  of  the 
retina,  and  only  in  the  very  last  stage  of  this  affection,  we 
find  the  retina  replaced  by  a  thin  layer  of  tough  connective- 
tissue  containing  some  blood-pigment,  and  in  no  way  resem- 
bling this  membrane.  This  I  saw  in  a  case  of  traumatic 
retinitis  twelve  years  after  the  beginning  of  the  disease. 

The  rods  and  cones,  as  already  stated,  are  usually  altered 
at  an  early  period.  They  mostly  appear  as  club-shaped 
structures,  as  we  found  them  in  cases  of  albuminuric  retinitis. 
According  to  several  authors,  hypertrophy  of  the  rods  and 
cones  as  described  above,  is  also  found  in  diffuse  interstitial 
retinitis  {Leber). 

The  blood-vessels  of  the  retina  gradually  become  quite 
obliterated  and  transformed  into  bands  of  connective-tissue, 
which  at  first  are  easily  distinguishable  from  the  surrounding 
tissue.  Later  on  this  distinction  becomes  impossible,  unless 
their  former  site  can  be  recognized  by  some  blood  pigment 
embedded  in  the  tissue. 


Sometimes  also,  in  this  form  of  retinitis,  the  pigmented  epi- 
thelial cells  proliferate  into  the  retina.  Diffuse  retinitis  which 
is,  however,  consequent  upon  the  immigration  of  pigmented 
epithelial  cells  into  the  retina,  and  above  referred  to  as  pig- 
mentary retinitis,  is  totally  different  because  a  secondary 
affection,  although  histologically  the  same,  changes  are  ob- 
served as  in  the  disease  now  under  consideration. 

c.  Retinitis  Puriilenta. 

Purulent  retinitis  is  in  most  cases  a  part  of  purulent 
panophthalmitis.  We  furthermore  observe  it  after  injuries 
which  involve  the  retina  directly  or  in  cases  of  metastatic 
choroiditis,  which  latter  disease  usually  leads  to  purulent 
panophthalmitis. 

The  first  symptom  characteristic  of  this  affection,  is  a  very 
considerable  infiltration  of  round-cells  into  the  nerve  fibre 
layer  consequent  upon  hyperaemia  of  the  blood-vessels.  On 
account  of  the  infiltration,  this  layer  appears  much  swollen. 
Its  normal  elements  are  gradually  destroyed,  and  at  a  later 
period  it  seems  to  consist  solely  of  round-cells,  separated  from 
the  vitreous  body,  by  the  internal  limiting  membrane,  which 
generally  appears  wrinkled.  Gradually  this  membrane,  too, 
is  destroyed  and  the  neighboring  parts  of  the  vitreous  body 
which  have  for  some  time  also  been  filled  with  round-cells, 
come  into  direct  contact  with  the  altered  nerve  fibre  layer 
of  the  retina.  During  this  process,  very  numerous  haemor- 
rhages of  varying  size  are  observed  in  the  retina.  According 
to  Leber  and  others,  th'ese  are  caused  by  capillary  embolism, 
which  opinion  is  as  yet  not  to  be  considered  proven.  It  is 
certain,  however,  that  the  walls  of  the  blood-vessels  take  an 
active  part  in  the  formation  of  round-cells,  and  it  appears  to 
me,  that  the  changes  in  the  structure  of  the  blood-vessels 
necessarily  caused  by  this  process,  very  easily  explain  the 
occurrence  of  the  haemorrhages. 

The  remainder  of  the  retina  is  generally  invaded  by  the 
disease  at  a  much  later  period  than  the  nerve  fibre  layer,  and 
it  is  very  difficult  to  distinguish,  when  the  formation  of 
round-cells  in  the  granular  layer  really  begins,  on  account  of 
the  similarity  of  their  cellular  elements  to  the  round-cells. 


178 


THE  HUMAN  E  YE. 


It  seems,  however,  that  the  radiating  fibres  are  the  first  to 
suffer,  and  that  the  process  only  later  on  spreads  upon  the 
cellular  elements. 

In  advanced  cases,  the  whole  of  the  retina  is  replaced  by 
a  mass  of  round-cells  leaving  no  trace  whatever  of  its  original 
structure.  Purulent  retinitis  is  generally  combined  with 
purulent  hyalitis,  and  it  is  then  impossible  to  discern  which 
part  of  the  round-cells  has  taken  the  place  of  the  retina. 
The  rods  and  cones  are  usually  changed  at  an  early  period. 
They  at  first  take  the  club-shaped  form  above  mentioned, 
and  later  on  are  totally  destroyed.  Frequently  we  find  in 
their  stead  a  layer  of  round-cells,  (which  probably  come  from 
the  choroid)  even  before  the  outer  layers  of  the  retina  are 
materially  altered. 

Circumscribed  accumulations  of  round-cells  in  the  retina 
have  recently  been  described  as  tubercles  by  Weiss. 

C.  Changes  in   the    Structure   of  the   Retinal  Blood-vessels, 
Hcemorrhages  and  Detachment  of  the  Retina. 

Besides  the  alterations  which  the  retinal  blood-vessels 
undergo  when  this  membrane  is  inflamed,  and  which  have  been 
described  above  as  general  ecstasia,  fatty  degeneration,  nar- 
rowing of  the  lumen  consequent  upon  swelling  and  hyaline 
degeneration  of  the  walls,  thrombosis  and  perivasculitis,  there 
are  a  few  such  alterations  which,  as  it  seems,  are  not  neces- 
sarily combined  with  an  inflammatory  process  in  the  retinal 
tissue. 

Small  aneurysms  of  the  retinal  arteries  are  but  rarely  ob- 
served. They  appear  either  as  spindle-shaped  or  diverticlum- 
like  enlargements  of  the  blood-vessels. 

In  one  single  case  I  found  an  amyloid  degeneration  of 
the  walls  of  the  retinal  blood-vessels  in  a  case  of  detachment 
of  the  retina,  caused  by  a  choroidal  sarcoma.  The  walls  of 
some  of  the  blood-vessels  appeared  perfectly  hyaline,  the 
walls  of  others  contained  only  a  number  of  aggregations  of 
a  hyaline  substance.  The  chemical  reaction,  produced  by 
iodine,  was  that  characteristic  of  amyloid  degeneration. 

Haemorrhages  in  the  tissue  of  the  retina  are  of  very  fre- 
quent occurrence.     We  had  already  several  times  occasion 


RETnVA. 


179 


to  mention  them.  They  are  found  without  any  inflammatory 
process  in  the  retinal  tissue  in  the  cases  which  have  chnically 
very  inappropriately  been  called  retinitis  apoplectica  and 
haemorrhagica.  They  result  from  disease  of  the  heart,  throm- 
bosis of  the  arteria  or  vena  centralis  retinae,  from  injuries  to 
the  eye-ball,  haemorrhagic  glaucoma  and  several  constitu- 
tional diseases.  They  are,  of  course,  in  no  way  different'from 
those  caused  by  the  different  varieties  of  retinitis  above  de- 
tailed, and  we  may  frequently  find  the  rupture  in  the  blood- 
vessel which  has  caused  them.  They  disappear  after  having 
undergone  a  fatty  degeneration  by  being  absorbed. 

Sometimes  the  haemorrhage  destroys  the  elements  of  the 
part  of  the  retina  in  which  it  occurs.  In  these  cases,  usually 
a  circumscribed  retinitis  is  found  to  follow,  which  leads  to 
the  formation  of  a  scar,  sometimes  containing  crystals  of 
blood-pigment. 

Deposits  of  lime  are  but  very  rarely  found  in  the  walls 
of  retinal  blood-vessels  and  chiefly  in  phthisical  eye-balls  and 
detached  retinae.  In  the  earliest  period  of  this  pathological 
process,  the  walls  of  the  blood-vessels  appear  infiltrated  with 
minute  granules.  Later  on,  larger  bodies  of  amorphous  lime 
are  found,  and  finally  entire  blood-vessels  may  be  seen 
changed  into  cylinders  of  lime.  (See  Fig.  92). 

The  various  methods  by  which  the  retina  may  become 
detached,  are  not  yet  definitely  ascertained,  and  it  is  not  the 
place  here  to  speak  more  extensively  about  this  subject  than 
has  already  been  done  in  the  foregoing  chapters,  as  we  are 
here  only  interested  in  the  pathological  changes  found  in  the 
tissue  of  the  detached  retina. 

As  we  stated  above,  the  retina  can  only  become  detached 
when  the  structure  of  the  vitreous  body  has  been  materially 
altered.  When  detachment  has  taken  place,  the  blood-ves- 
sels of  the  retina  are  twisted  and  bent  in  many  ways  so  that 
we  may  a  priori  assume  that  the  nutrition  of  the  detached 
membrane  must  be  considerably  impaired,  even  if  there  are 
no  pathological  changes  present  in  the  uveal  tract.  The 
latter  is,  however,  usually  the  case. 

The  result  of  this  impairment  of  nutrition  also  undoubt- 
edly of  the  loss  of  function,  is  a  regressive  metamorphosis  of 


i8o 


THE  HUMAN  E  YE. 


the  nervous  elements  of  the  retina.  The  elements  undergo 
a  fatty  degeneration,  sometimes  also  a  colloid  metamorpho- 
sis, which  may  give  rise  to  the  formation  of  larger  cystoid 
structures.     Meanwhile   the    connective-tissue    has    become 


Fig.  9a.  -Detached  and  perfectly  atrophied  retina.    Capillaries  changed  into  cylinders  of 

amorphous  lime. 

hyperplastic,  and  later  on  we  find  all  the  symptoms  of  diffuse 
interstitial  (atrophic)  retinitis.  The  blood-vessels  are  tran.s- 
formed  into  bands  of  connective-tissue,  or  sometimes,  as 
stated  above,  into  cylinders  of  amorphous  lime,  and  often  we 
can  recognize  their  former  site,  only  by  the  remains  of  the 
blood  pigment. 

While  the  whole  of  the  structure  of  the  retina  is  thus  per- 
fectly destroyed  and  replaced  by  connective-tissue,  the  limi- 
tans  interna  is  always  found  intact  between  the  folds  of  this 
new  tissue.  This  fact,  combined  with  all  the  reasons  already 
mentioned,  proves  the  limitans  interna  to  be  undoubtedly  a 
separate  and  independent  membrane. 

Sometimes  we  find  detached  with  the  retina  and  lying 
within  this  membrane,  vitreous  bodies  from  the  lamina  vitrea 
of  the  choroid.  They  may  contain  lime,  and  lead  to  ossifi- 
cation in  the  atrophic  retina. 

The  Results  of  Retinitis. 
In  rare  cases  we  may  clinically  observe  that  all  the  symp- 


RETINA.  l8l 

toms  of  albuminuric  retinitis  disappear.  It  appears  doubtful 
also  whether  histologically,  a  perfect  restitutio  ad  integrum, 
especially  when  the  disease  has  reached  an  advanced  state,  is 
possible.  The  final  changes  caused  by  albuminuric  retinitis 
are,  it  seems  not  known.  This  is  easily  explained  by  the 
fact  that  death  nearly  always  results  from  the  primary  disease, 
while  the  retinitis  is  as  yet  progressing.  If  we  find  in  a  retina 
sclerotic  hypertrophy  of  the  nerve  fibres,  fatty  degeneration, 
oval  cavities  filled  with  fibrine,  or  the  cells  containing  fat- 
granules  and  above  described,  sclerosis  of  the  walls  of  the 
blood-vessels  and  numerous  haemorrhages,  we  are  justified  in 
making  the  diagnosis  of  albuminuric  retinitis.  We  shall,  how- 
ever, always  find  that  the  inflammatory  process  is  not  yet  at 
an  end. 

The  changes  which  occur  after  diffuse  interstitial  retinitis, 
are  different.  The  chief  symptom  of  this  disease  is  the 
transformation  of  the  retina  into  connective-tissue,  and  par- 
tial or  total  destruction  of  the  nervous  elements. 

If  the  process  had  come  to  an  end  during  life,  we  find  the 
retina  replaced  by  a  very  thin  membrane,  consisting  of  tough 
connective-tissue  which  usually  contains  some  haematoidine 
crystals  and  uveal  pigment.  This  membrane  can  only  be 
recognized  as  the  former  retina  by  its  position  in  the  eye- 
ball. 

I  frequently  found  in  phthisical  eye-balls  or  eyes  which 
had  been  blind  for  a  long  period  before  death  occurred,  the 
nerve  fibre  layer  of  the  retina  abnormally  thin,  and  some 
new-formation  of  connective-tissue  going  on  within  it ; 
furthermore,  some  ganglionic  cells  undergoing  fatty  or  colloid 
metamorphosis,  and  the  cells  of  the  granular  layers  in  a  state 
of  molecular  infiltration.  I  think  these  alterations  are  due 
to  the  loss  of  function,  and  cannot  be  considered  as  the  symp- 
toms of  a  diffuse  interstitial  retinitis. 

In  consequence  of  purulent  retinitis,  the  retina  is  also 
usually  entirely  destroyed,  and  we  are  often  unable  to  find  a 
trace  of  it  in  eyes  which  have  been  lost  from  purulent  pan- 
ophthalmitis. This  is  more  particularly  the  case,  if  the 
vitreous  body  too  has  been  altered  into  a  mass  of  round- 
cells. 


1 82  THE  HUMAN  EYE. 

D.  Injuries  to  the  Retina  and  their  Results. 

The  position  of  the  retina  inside  the  eye-ball,  of  course, 
does  not  allow  of  any  direct  injuries  being  inflicted  upon 
it,  unless  other  parts  have  first  been  perforated.  The  most 
frequent  and  most  important  combination,  is  simultaneous 
injury  of  retina,  choroid  and  vitreous  body.  We  had 
already  occasion  to  speak  of  these  injuries  when  treating  upon 
the  conditions  found  after  injuries  to  the  choroid. 

Injuries  to  the  retina  mostly  produce  a  circumscribed  in- 
terstitial retinitis.  The  tissue  of  the  lips  of  the  wound  is  at 
first  found  to  be  infiltrated  with  red  and  white  blood-corpus- 
cles, and  the  wound-canal  is  filled  with  a  fibrinous  coagulum, 
especially,  if  the  choroid,  too,  has  been  wounded.  The  white 
blood-corpuscles  then  increase  in  number,  invade  the  fibrinous 
coagulum  and  gradually  lead  to  the  formation  of  connective- 
tissue.  Such  scars  seems  afterwards  always  to  contain  some 
blood  pigment.  Sometimes  we  also  find  that  the  pigmented 
epithelial  cells  have  proliferated  into  the  scar.  This  is  espe- 
cially the  case,  when  the  choroid  is  injured  also.  In  the 
neighborhood  of  the  scar  the  rods  and  cones  are  destroyed, 
and  retina  and  choroid  are  as  a  rule  firmly  adherent  to  each 
other.  Berlin  also  found  sclerosed  hypertrophic  nerve  fibres, 
like  those  described  above,  near  such  retinal  wounds. 

We  stated  already,  that  granulation  tissue  may  start  from 
the  wounded  choroid,  and  grow  through  the  wound  canal  of 
the  retina  into  the  vitreous  body.  If  the  vitreous  body  has 
been  injured,  connective-tissue  is  formed  in  it,  also  near  the 
retinal  wound,  and  thus  we  find  retina  and  vitreous  body 
firmly  united  at  the  site  of  the  wound  at  a  later  period. 

In  rare  cases,  injuries  inflicted  upon  the  retina  will  cause 
purulent  retinitis,  which,  as  we  have  stated,  may  lead  to  the 
perfect  destruction  of  this  membrane.  It  is  usually  accom- 
panied by  purulent  choroiditis,  which  finally  leads  to  pan- 
ophthalmitis. 

Although  foreign  bodies  may  be  retained  in  the  retina, 
they  are  but  seldom  seen  to  become  encapsuled  in  this  mem- 
brane, as  they  mostly  cause  a  purulent  retinitis.  If,  however, 
they  become  encapsulated,  they  are  surrounded  by  a  dense 


RETINA. 


183 


connective-tissue,  in  the  formation  of  which  the  choroid  and 
vitreous  body  usually  take  an  active  part. 

E.  TUMORS   OF   THE   RETINA. 

a.  Fibroma. 

Some  authors  described  small  new-formations  upon  the 
inner  surface  of  this  membrane  as  fibromatous  tumors. 
These  are,  however,  probably  not  what  we  would  call  a  real 
tumor  of  the  retina,  but  new-formations  of  connective-tissue 
in  the  outer  layers  of  the  vitreous  body  or  hypertrophic 
radiary  jfibres  which  have  perforated  the  inner  limiting  mem- 
brane in  the  way  above  referred  to  and  observed  in  cases  of 
diffuse  interstitial  retinitis. 

The  conditions  seem  to  be  different,  however,  in  the 
cases  of  teleangiectatic  fibromatous  tumors,  which  we  find 
drawn  in  PagenstecJier  s  and  GentJi  s  atlas.  They  are  small 
tumors  with  a  broad  base  or  a  thin  pedicle,  and  are  very  vas- 
cular. 

b.  Small-celled  Medullary  Sarcoma  {Glioma^. 

During  the  infantile  age,  the  retina  is  often  the  seat  of  a 
new-formation,  which  was  formerly  described  as  fungus 
haematodes,  by  Virchow  and  his  followers,  as  glioma.  Vir- 
chow  called  this  new-formation  glioma,  because  it  originates 
in  the  soft  connective-tissue  of  the  retina,  which  is  analogous 
to  the  neuroglia  of  the  brain,  and  because  it  appears  to  be 
identical  with  the  brain  tumors  described  as  gliomata.  Virchow 
himself  stated  that  it  is  very  difficult  to  distinguish  between 
glioma  and  sarcoma,  and  overcame  the  difficulty  by  calling 
some  of  these  tumors  glio-sarcomata.  Most  of  the  recent 
authors  have  adopted  this  name  for  the  tumors  under  con- 
sideration. Delafield  has  recently  called  them  sarcomata  of 
the  retina,  being  forced  to  do  so  by  the  result  of  a  number 
of  examinations  of  such  retinal  tumors  both  in  a  fresh  con- 
dition, and  after  being  hardened.  I  too,  am  convinced  that, 
if  we  want  to  call  them  gliomata  still,  we  cannot  consider 
them  as  anything  else  than  sarcomata.  Leber,  too,  seems  to 
be  of  this  opinion. 


1 84  ^'^-^  HUMAN  EYE. 

All  the  different  authors  {Virchozu,  Schweigger,  Knapp, 
Hirschberg,  Delafield,  Leber,  etc.)  agree  in  the  description  of 
the  structure  and  elements  of  these  new-formations,  and  I  can 
add  nothing  new  to  their  observations.  They  consist  of 
round-cells,  which  are  sometimes  smaller,  sometimes  larger 
than  white  blood-corpuscles,  or  in  other  cases  are  perfectly 
identical  with  them.  When  hardened,  they  have  a  large 
round  nucleus.  Sometimes  these  cells  have  one  or  more  off- 
sets. It  has  been  stated  by  some  authors,  that  they  are  iden- 
tical with,  and  derived  from  the  nuclei  of  the  granular  layers, 
which  however,  is  not  the  case.  Between  these  round-cells 
we  find  free  nuclei  and  sometimes  very  much  larger  round 
and  even  spindle-cells.  The  tumors  in  which  these  spindle- 
cells  have  been  found,  have  more  especially  been  called  glio- 
sarcomata. 

The  cells  of  the  tumor  are  embedded  in  a  very  small 
quantity  of  intercellular  substance,  which  when  fresh  is  gran- 
ular. Knapp  states  that  this  granular  appearance  is  caused 
by  the  hardening  fluid. 

The  tumors  under  consideration  are  sometimes  very  vas- 
cular. The  blood-vessels  (mostly  of  a  capillary  character), 
are  unusually  wide.  They  take  their  origin  from  the  retinal 
blood-vessels. 

Sarcomata  of  the  retina  are  said  to  originate  sometimes 
from  the  inner,  sometimes  from  the  outer  granular  layer, 
in  a  few  cases,  also  from  the  nerve  fibre  layer.  Leber  found 
primary  tumors  at  the  same  time  in  different  layers,  and 
Livajioffxs  of  the  opinion,  in  which  I  concur,  that  the  tumor, 
being  a  connective-tissue  growth,  may  spring  from  the  con- 
nective-tissue elements  of  all  the  layers  of  the  retina.  It 
seems,  however,  that  it  most  frequently  starts  from  the  outer 
layers,  and  we  may  sometimes  find  the  inner  layer  as  yet 
perfectly  intact,  when  the  outer  ones  have  already  been  per- 
fectly destroyed  by  the  new-formation.  In  these  cases,  the 
retina  seems  to  be  always  detached,  and  lying  nearer  the  axis 
of  the  eye-ball.  There  are  however,  cases  in  which  the  retina 
may  remain  in  contact  with  the  choroid,  and  the  tumor 
spread  inwardly.  Delafield  has,  moreover,  described  a  case, 
in  which  the  tumor  originated  from  the  inner  granular  layer. 


RETINA. 


185 


and  had  protruded  into  the  vitreous  chamber,  while  the  rods 
and  cones  were  as  yet  found  to  be  perfectly  intact. 

During  the  growth  of  the  tumor,  haemorrhages  fre- 
quently take  place,  and  as  their  results,  we  find  smaller 
and  larger  patches  of  blood-pigment.  This  pigment  is 
either  enclosed  in  cells,  or  hes  between  them  in  the  shape 
of  crystals  or  as  an  amorphous  substance.  Fatty  infiltration, 
a  complete  fatty  softening,  and  the  formation  of  cheesy  mat- 
ter, is  not  infrequently  found  in  some  parts  of  these  tumors, 
and  generally  is  accompanied  by  the  formation  of  deposits 
of  lime.  We  find  either  minute  granules  of  lime  enclosed  in 
the  cells,  or  free  larger  roundish  bodies  which  may  coalesce, 
and  so  grow  to  a  considerable  size. 

The  tumor,  like  all  sarcomata,  may  spread  continuously, 
or  produce  secondary  nodules  by  infection  at  some  distance 
from  the  primary  ones.  The  former  seems  to  be  the  preva- 
lent manner  of  their  growth  in  the  retina,  and  the  tumor  may 
thus  grow  all  over  the  retina,  spread  to  the  optic  nerve  and 
even  to  the  choroid,  after  an  adhesion  between  retina  and 
choroid  has  taken  place  (Knapp).  The  second  mode  of 
growth  is  generally  the  origin  of  isolated  secondary  tumors 
found  in  the  choroid,  the  sclerotic  and  the  episcleral  tissue. 
Furthermore,  metastatic  tumors  have  been  observed  in  the 
bones,  the  lymphatic  glands,  the  liver  and  other  organs. 

While  the  eye-ball  is  gradually  being  filled  by  the  new- 
formation,  the  intra-ocular  pressure  becomes  increased. 
This  together  with  the  impairment  in  nutrition  of  the  anterior 
portions  of  the  eye-ball,  causes  the  formation  of  abscesses  in 
the  cornea,  and  leads  to  the  total  destruction  of  this  mem- 
brane, thus  opening  a  channel  by  which  the  tumor  can  spread 
upon  the  outer  surface  of  the  eye.  The  tumor  but  seldom 
perforates  the  sclerotic. 

When  the  eye-ball  is  perfectly  filled  by  the  new-formation, 
the  whole  of  the  uveal  tract  may  be  destroyed  and  entirely 
disappear,  leaving  only  small  quantities  of  pigment  behind. 

From  this  description  it  seems  evident,  that  the  so-called 
glioma  of  the  retina  in  no  way  differs  histologically  from  the 
medullary  small-cell  sarcomata.  I  therefore  see  no  reason 
why  we  should  not  call  these  new-formations  by  that  name. 


1 86  THE  HUMAN  EYE. 

Some  few  cases  have  been  described,  in  which  glioma  is 
said  to  have  disappeared  by  a  general  shrinking  of  the  eye- 
ball. From  these  observations,  the  new-formation  has  been 
thought  to  be  of  a  fibromatous  character.  The  observations 
are,  however  doubtful  on  the  one  hand,  and  on  the  other  a 
very  considerable  number  of  so-called  glioma  of  the  retina 
have  up  to  this  date  been  examined  without  proving  this 
opinion  to  be  the  correct  one. 


IX. 

LENS   CRYSTALLINEA. 

I.  Normal   Conditions. 

The  crystalline  lens  is  fastened  to  the  ciliary  body  by 
means  of  the  zonula  of  Zimi,  which  encloses  the  canalis 
Petilii,  consists  of  the  lens-capsule,  the  capsular  epithelium 
and  the  lens-fibres. 

The  lens-capsule  forms  a  sac  in  which  the  remainder  of 
the  elements  constituting  the  crystalline  lens  are  enclosed. 
The  clinical  distinction  between  an  anterior  and  a  posterior 
lens-capsule  is  not  histologically  justifiable. 

The  lens-capsule  is  a  perfectly  transparent  membrane, 
which  is  not  equal  in  thickness  in  all  its  parts.  It  is  thickest 
at  and  around  the  anterior  pole  of  the  crystalline  lens,  and 
thinnest  upon  its  posterior  surface,  especially  at  the  posterior 
pole.  The  lens-capsule  is  generally  thicker  in  advanced  age 
than  in  youth. 

In  plain  views  it  appears  perfectly  homogeneous.  A 
number  of  authors  have  seen  a  fine  striation  upon  its  trans- 
verse section,  which  I  have  never  been  able  to  recognize. 
Such  a  lamellar  structure  would,  however,  be  sure  proof  of 
the  connective-tissue  character  of  the  lens-capsule,  of  which 
I  have  no  doubt,  as  it  is  analogous  in  every  way  to  Dcscemefs 
membrane  and  the  lamina  vitrea  choroideae. 

As  has  been  stated  by  a  great  many  authors,  the  lens- 
capsule  is  an  elastic  membrane.  If  ruptured  or  partially  de- 
tached from  the  lens  substance,  it  will  roll  itself  up.  From 
experiments  on  the  eyes  of  animals,  I  had  formed  the  opinion 
that  the  lens-capsule  would  always  roll  itself  up  in  a  centri- 
fugal direction,  I  have,  however,  since  then  seen  the  human 
lens-capsule  to  be  rolled  up  in  a  centrifugal  as  well  as  a  cen- 
tripetal manner.  The  lens-capsule  may  furthermore  simply 
retract  and  thus  become  wrinkled. 

The  capsular  epithelium  is  a  single  layer   of  epithelial 


1 8  8  THE  H  UMA  N  E  YE. 

cells,  lying  on  the  inner  surface  of  the  anterior  lens-capsule, 
which  appear  hexagonal  in  a  plain  view,  similar  to  the 
endothelium  oi  Descetnet's  membrane.  Each  cell  has  a  large 
round  or  oval  nucleus.  IVed/  and  HoscJi  have  also  described 
cells  with  hyaline  offsets.  These  cells  are  united  by  a  small 
quantity  of  cementing  substance,  which  is  easily  seen  when 
stained  with  nitrate  of  silver.  At  the  equator  of  the  lens 
these  epithelial  cells  grow  longer  and  appear  like  cylinder 
cells,  and  gradually  form  the  so-called  lens  fibres.  The  pos- 
terior lens-capsule,  that  is,  the  portion  of  the  lens-capsule 
which,  beginning  at  the  equator,  covers  the  posterior  surface 
of  the  lens  substance,  has  no  epithelium.  Some  authors  have 
been  misled  into  the  description  of  such  an  epithelium  by 
hardened  cementing  substance,  or  by  the  ends  of  lens  fibres 
attached  to  it. 

The  cells  of  the  capsular  epithelium  are  all  somewhat 
granular.  According  to  y.  Arnold,  this  granular  appearance 
is  more  pronounced  near  the  equator,  while  the  outlines  of 
the  cells  there  grow  less  distinct. 

I  have  never  seen  any  new-formation  of  cells  in  the  nor- 
mal capsular  epithelium. 

The  bulk  of  the  crystalline  lens  is  formed  of  the  lens- 
fibres  or  lens-bands  (y.  Arnold^.  Isolated  lens-fibres  when 
lying  flat,  appear  as  broad  bands,  and  are  striated  in  a  longi- 
tudinal direction.  The  transverse  striation  which  has  been 
described  by  a  number  of  authors,  I  never  found  in  normal, 
but  sometimes  in  pathological  lenses.  When  the  lens-fibres 
lie  on  their  edge,  they  appear  much  narrower.  Their  real 
shape  is  best  seen  in  transverse  sections,  and  we  then  find 
them  to  be  hexagonal  prisms.  They  vary  in  size,  and  those 
taken  from  the  centre  of  the  crystalline  lens  are  usually 
smaller  than  those  taken  from  its  periphery.  The  lens- 
fibres  taken  from  the  centre  have,  moreover,  especially  at  an 
advanced  age,  no  nucleus,  while  those  from  the  periphery 
always  have  an  oval  nucleus  lying  with  its  long  axis  in  the 
direction  of  the  lens-fibre.  Every  such  lens-fibre  contains 
only  one  nucleus,  and  the  statements  with  regard  to  fibres 
with  two  and  more  nuclei,  do  not  seem  to  be  correct. 

The  body  of  the  peripheral  lens-fibres  seems  to  consist 


LEA'S  CRYSTALLIKEA.  i8q 

of  two  parts  ;  a  tough  peripheral  and  a  softer  central  part. 
The  latter  is  formed  of  myeline,  and  called  liquor  Morgagni 
The  nearer  the  centre  of  the  lens-fibres,  the  more  of  the 
harder,  tougher  substance,  and  the  less  liquor  Morgagni  is 
found.  On  their  narrow  sides,  the  margins  of  the  lens-fibres 
are  indented.  This  indentation  is  according  to  J.  Arnold's 
statement,  more  pronounced  in  the  central  fibres,.-and  grad- 
ually disappears  towards  the  periphery.  The  little  offsets  of 
the  neighboring  lens-fibres  interlace  like  those  of  the  bones  of 
the  skull.  All  the  fibres  are  united  with  each  other  by  a 
cementing  substance,  which  when  fresh  is  homogeneous  or 
slightly  granular,  and  can  be  well  recognized  when  stained 
with  nitrate  of  silver.  I  never  saw  as  beautiful  regular  hexag- 
onal figures  in  a  transverse  section  of  the  lens-fibres  as 
J.  Arnold  has  drawn.  The  lines  produced  by  the  stained 
cementing  substance  have  always  appeared  wavy  in  my  speci- 
mens. Where  the  ends  of  the  lens-fibres  touch  each  other 
upon  the  anterior  and  posterior  surface  of  the  crystalline 
lens,  they  form  the  so-called  lens-stars.  In  the  newly-born, 
these  stars  each  consist  of  three  lines  which  lie  at  angles  of 
about  one  hundred  and  twenty  degrees  to  each  other,  and  are 
united  in  the  anterior  and  posterior  pole.  While  two  of 
these  lines  on  the  anterior  surface  run  upwards  and  one 
downwards,  the  condition  is  the  reverse  one  upon  the  poste- 
rior surface.  These  lines  never  reach  the  equator,  and  end  in 
what  has  been  called  the  "  fibre-vortex."  In  the  adult,  they 
branch  off  into  secondary  ones.  In  very  old  lenses  we  find 
these  lines  changed  into  fissures  filled  with  liquor  Morgagni. 
The  lens  fibres  as  they  approach  these  lines,  are  a  little 
broader  and  bent. 

According  to  J.  Arnold,  the  lens-fibres  in  a  meridional 
direction,  have  the  shape  of  a  Roman  S,  from  the  back 
towards  the  front,  but  they  never  entirely  reach  from  one  pole 
to  the  other. 

If  we  divide  the  lens  by  cutting  through  both  its  poles, 
and  vertically  upon  the  equator,  we  see  that  the  most  peri- 
pheral lens-fibres  are  convex  towards  the  centre  ;  this  convex- 
ity is  gradually  changed  into  the  opposite  direction,  as  the 
fibres  come  nearer  the  centre.     The  nuclei  of  the  lens-fibres 


J  90 


THE  HUMAN  E  YE. 


appear  in  such  a  section  arranged  in  such  a  way,  as  to  form 
a  line  which  is  convex  towards  the  anterior  surface  of  the 
crystalh'ne  lens  and  lies  near  it. 

2.  Pathological  Conditions. 

The  tissue  of  the  crystalline  lens  does'  not  become  in- 
flamed like  other  tissues.  Although  Iwanoff  and  Becker 
have  described  a  hyperplastic  process  in  the  capsular  epithe- 
lium as  taking  place  within  the  perfectly  intact  lens-capsule, 
and  called  it  phakitis,  I  have  never  been  able  to  see  it. 
According  to  Rvanoff,  the  "  new-formed  cells  are  much  larger 
and  the  nucleus  easily  divides  itself  into  two  and  more.'' 
Furthermore,  these  cells  are  said  "  to  be  very  prone  to  under- 
go a  colloid  or  mucoid  metamorphosis,  and  then  to  form  large 
vesicles,  filled  with  colloid  substance,  which  crowd  the  nucleus 
to  one  side."  These  vesicles,  which  Becker  calls  giant-cells, 
seem  to  me  to  be  identical  with  the  myeline  globules  of  which 
we  shall  speak  farther  on,  and  which  never  contain  a  nucleus. 
The  pathological  changes  of  the  crystalline  lens  when  the 
capsule  is  intact,  and  which  are  called  cataract,  are  simply 
regressive  metamorphoses  of  the  elements  constituting  the 
crystalline  lens.  We  find  frequently  the  anterior  capsule  of 
such  pathological  crystalline  lenses  very  much  thickened. 
Transverse  sections  of  such  thickened  capsules,  show  it  to  be 
either  perfectly  homogeneous,  or  to  possess  a  longitudinal 
striation  {Babuchin,  Becker). 

Atrophy  of  the  lens-capsule,  which  H.  Mueller  and  Becker 
have  described,  has  never  come  under  my  own  observation, 
and  the  thickness  of  the  lens-capsule  varies  so  much  in  differ- 
ent individuals,  that  such  an  atrophy  must  be  very  difficult 
to  diagnose. 

The  deposits  upon  the  outer  surface  of  the  anterior  and 
posterior  lens-capsule,  caused  by  iritis  and  cyclitis,  do  not 
belong  among  the  pathological  changes  of  the  crystalline 
lens. 

A.  Cataract  formed  within  an  Intact  Lens-capsule. 

It  is  possible  to  distinguish  both  clinically  and  anatomi- 
cally between  a  large  number  of  cataracts,  since  the  dimness 


LE.VS  CRYSTALLINEA.  Igi 

caused  by  regressive  metamorphosis  of  the  lens  fibres,  may 
have  a  varying  shape,  and  lie  in  very  different  regions.  The 
histological  conditions  are  the  same  in  nearly  all  of  these  cases 
and  we  can  only  distinguish  between  cataract  caused  by 
physiological  progressive  sclerosis  of  the  lens  fibres,  and 
that  caused  by  a  pathological  regressive  metamorphosis  of 
these  elements. 

As  above  stated,  the  central  lens  fibres  when  in  a  normal 
condition  are  harder  than  the  peripheral  ones,  and  have  no 
nucleus.  This  central  sclerosis,  like  the  formation  of  horny 
scales  on  the  surface  of  the  epithelium  of  the  skin,  is  pro- 
gressive, and  gradually  spreads  towards  the  periphery  in  such 
a  way,  that  more  and  more  lens  fibres  become  sclerosed,  until 
finally  all,  or  nearly  all  of  them  are  thus  altered.  At  the 
same  time,  small  quantities  of  liquor  Morgagni  are  found  to 
lie  outside  the  lens  fibres.  They  form  round  and  oval  drops 
of  a  varying  size,  and  lie  chiefly  between  the  ends  of  the 
lens  fibres.  The  latter  elements  appear  very  brittle,  no  longer 
have  any  nucleus,  and  in  transverse  sections  we  see,  that  they 
have  lost  their  comparatively  regular  hexagonal  shape,  are 
sometimes  perfectly  cylindrical,  and  no  longer  indented  at 
their  margins.  When  all  the  fibres  have  been  thus  altered, 
we  call  the  condition  clinically  a  mature  senile  cataract 
(cataracta  nigra).  Frequently,  however,  we  find  in  these 
cataracts  a  larger  quantity  of  free  myeline  globules  (liquor 
Morgagni )  and  a  part  of  the  lens  is  accordingly  more  fluid 
(especially  the  peripheral  layers). 

This  hard  cataract  caused  by  the  physiological  progressive 
sclerosis  is  seldom,  if  ever  stationary,  and  the  fibres  usually 
undergo  a  further  regressive  metamorphosis,  that  is,  the  catar- 
act becomes  what  we  clinically  call  hypermature.  These 
regressive  metamorphoses  are,  however,  also  found  without 
preceding  sclerosis,  and  are  the  histological  factors  causing 
all  other  kinds  of  cataract,  especially  those  found  congenitally 
or  in  young  people. 

In  such  cataracts  we  find  beside  the  globules  of  liquor 
Morgagni,  that  the  lens  fibres  are  at  first  granular,  which  is 
the  beginning  stage  of  fatty  degeneration.  Later  on,  the 
molecular  granules  are  changed  into  larger  drops  which  coa- 


192 


THE  HUMAN  EYE. 


lesce.  In  this  way  the  whole  of  the  lens  substance  may  be- 
come fluid,  and  then  consists  of  liquor  Morgagni  and  fat- 
globules.  The  existence  of  the  latter  is  especially  proven 
by  the  formation  of  cholestearine  crystals,  which  may  be  found 
in  such  cataracts.  Sometimes  we  also  see  myeline  drops 
filled  with  crystals  of  margaric  acid.  In  other  cases,  a  num- 
ber of  lens  fibres  which  are  not  yet  perfectly  broken  up,  are 
found  to  have  spindle-shaped  enlargements  which  phenome- 
non is  probably  caused  by  imbibition. 

In  rare  cases  (according  to  Iwanoff  always)  lens  fibres, 
before  being  broken  up,  may  be  found  to  have  a  transverse 
striation.  This  striation  resembles  that  of  the  muscular 
fibres,  from  which  it  is,  however,  distinct,  since  the  striae  do 
not  lie  at  regular  intervals,  and  do  not  cross  the  longitudinal 
direction  of  the  fibres  at  right  angles. 

In  most  of  the  cases  of  soft  cataract,  we  find  lens  fibres  in 
all  stages  of  destruction.  Even  where  the  clinical  appear- 
ance would  seem  to  justify  the  idea  that  all  of  the  lens  fibres 
must  be  destroyed,  we  may  yet  find  normal  ones  and  others 
which,  although  they  are  granular,  have  not  yet  lost  their 
normal  shape. 

During  the  destruction  of  the  lens  fibres,  lime  may  be  de- 
posited in  the  lens.  Becker  s  statement,  however,  that  lime 
is  only  deposited  in  a  place  where  the  lens  fibres  have  been 
altogether  destroyed,  is  not  correct.  I  have  in  my  possession 
some  specimens  of  a  lens  which  show  only  the  symptoms 
of  senile  sclerosis  with  a  quantity  of  deposits  of  lime. 

The  lime  is  found  in  small  granules  which  coalesce  and 
thus  form  larger  bodies.  These  may  also  again  coalesce,  but 
even  very  large  accumulations  of  lime  retain  the  granular 
structure. 

During  all  these  changes,  the  capsular  epithelium  may 
either  remain  unaltered,  or  it  is  gradually  destroyed  by  fatty 
degeneration. 

As  mentioned  above,  Iwajioff,  H.  Mueller  and  Becker  de- 
scribed a  new-formation  of  cells  in  the  capsular  epithelium. 
Becker  says  that  this  new-formation  may  appear  later  on  as 
a  tissue  consisting  of  spindle-shaped  cells,  and  more  than  ten 
times  as  thick  as  the  normal  capsular  epitheliiiiii.     I   have 


LENS  CR  YSTALLINEA. 


193 


never  seen  this  tissue  or  any  new-formation  of  the  cells  of  the 
capsular  epithelium  where  the  lens-capsule  was  perfectly 
intact  ;  I  shall  however,  later  on  have  to  describe  a  perfectly 
similar  cell  new-formation  found  when  the  lens-capsule  has 
been  ruptured.  Perhaps,  this  was  also  the  case  with  the 
lenses  in  which  Becker  saw  these  changes. 

Furthermore,  he  mentions  the  formation  of  "  giant-cells," 
and  states  expressly  that  they  could  not  possibly  be  myeline 
globules,  since  they  have  a  nucleus.  He  found  them,  espe- 
cially in  cases  of  cortical  cataract,  in  dislocated  lenses,  in 
traumatic  and  secondary  cataracts.  I  must  state  that  I  have 
never  seen  these  cell  formations.  I  have,  however,  very  fre- 
quently thought  I  saw  a  nucleus  in  such  large  myeline-globules 
and  convinced  myself  only  by  further  examination,  that  I  was 
deceived  by  another  smaller  globule  lying  above  or  under-' 
neath  the  larger  one.  Sometimes  the  myeline-globules  have 
also  a  double  contour,  and  it  may  thus  appear  as  if  we  had  to 
do  with  a  cell  membrane. 

The  formation  of  pus-cells  in  the  lens  substance,  while  the 
capsule  was  unruptured,  has  only  once  been  seen  by  Knapp. 
Becker  has  never  seen  it,  and  I  have  looked  for  it  in  vain, 
even,  in  cases  of  purulent  panophthalmitis,  and  when  the  lens- 
capsule  was  ruptured. 

Two  varieties  of  cataract  formed  inside  of  a  perfectly  intact 
capsule  are  yet  to  be  mentioned,  as  showing  some  peculiar 
histological  conditions  ;  I  mean,  cataracta  polaris  anterior 
(pyramidalis)  and  cataracta  haemorrhagica. 

Cataracta  polaris  anterior  (pyramidalis)  is  formed  by  a  cone 
which  lies  upon  the  normal  lens  substance  in  the  region  of  the 
anterior  pole.  This  cone  is  always  covered  with  lens-capsule, 
and  the  latter  accordingly  has  a  diverticalum  in  which 
the  cone  lies.  The  normal  capsular  epithelium  reaches  up 
to  the  base  of  this  cone.  According  to  Becker,  the  apex  of 
the  cone  is  filled  with  coagulated  fluid,  while  nearer  the  base 
he  found  a  tissue  consisting  of  spindle-shaped  cells,  very  simi- 
lar to  the  tissue  of  the  cornea.  H.  Mueller  and  Schweigger 
found  the  cone  to  consist  of  a  fatty  cretaceous  substance,  in 
which  H.  Mueller  could  not  find  any  cellular  elements. 
Hiilke  also  states  that  cells  are  found  in  this  substance.     I 


194 


THE  HUMAN  EYE. 


had  occasion  to  examine  one  such  cataract.  The  cone  was 
also  in  this  case  enclosed  in  the  wrinkled  lens-capsule,  and 
two-thirds  of  it  consisted  of  a  lamellar  substance  without  any 
cellular  elements.  Its  basis  was  formed  by  fat-drops  and 
lime  granules,  and  reached  below  the  level  of  the  surrounding 
normal  capsular  epithelium.  (See  Fig.  93). 


Fjg.  93. — Anterior  polar  cataract.    The  apex  of  the  cone  is  formed  by  a  lamellar,  dim 
tissue,  without  any  cellular  elements.    The  basis  consists  of  lime  and  fat. 

Haemorrhagic  cataract  has  been  once  examined  and  de- 
scribed by  von  Groefe.  He  found  the  lens  fibres  brown, 
which  color  was  caused  by  granular  and  crystallized  blood- 
pigment  within  them,  while  their  shape  was  unaltered.  The 
capsular  epithelial  cells  too,  were  filled  with  the  pigment. 
It  could  not  be  ascertained  in  this  case  whether  the  lens-cap- 
sule was  intact  or  ruptured. 

Wagner  and  Lohmayer  have  described  the  formation  of 
osseous  tissue  within  the  lens-capsule.  Whether  the  capsule 
was  ruptured  or  not,  is  not  stated.  More  recently  Voorhies 
again  described  such  an  ossification  of  the  lens  substance,  but 
omitted  to  state  anything  regarding  the  state  of  the  lens-cap- 
sule. ^^^>^iT  draws  attention  to  the  fact,  that  ossification  in  a 
cyclitic  membrane  might  easily  lead  to  deception,  and  be  taken 
for  ossification  of  the  crystalline  lens.  I  shall  later  on  also  have 
to  refer  to  the  formation  of  osseous  tissue  within  the  lens- 
capsule,  which  I  found,  however,  always  to  be  ruptured.  A 
direct  change  of  epithelial  tissue,  like  the  lens  fibres,  into 
osseous  tissue  has  not  yet  been  definitely  observed. 

B.  Injuries  to  the   Lens-capsule  a?id  the  Lens-substance   and 
their  Results. 

Single  small  wounds  of  the  lens-capsule  can,  as  it  appears 
from  Ritters  experimental  observations,  heal  by  simple  repo- 
sition of  the  lips  of  the  wound.     Becker  states,  that  by  seeing 


LENS  CRYSTALLINEA, 


195 


specimens  oi  Leber  s,  he  came  to  the  conclusion  that  such  small 
wounds  of  the  capsule  may  heal  with  the  new-formation  of  a 
small  amount  of  vitreous  substance,  analogous  to  the  capsular 
substance,  and  that  the  capsular  epithelial  cells  do  7iot  take 
part  in  the  production  of  this  new-formation.  This  is  a 
remarkable  observation,  as  we  know  that  similar  wounds  of 
Desceinefs  membrane  never  heal.  I  am  however,  not  in  the 
position  to  criticise  Becker  s  statement,  as  I  do  not  possess 
any  similar  specimens. 

(At  the  last  meeting  of  oculists  at  Heidelberg,  1878, 
Leber  showed  such  specimens  from  the  crystalline  lens  of 
rabbits.  He  came  to  the  conclusion,  however,  that  the 
capsular  epithelial  cells  produced  the  newly  formed  glass  sub- 
stance. He  stated  that  these  cells  proliferate  into  the  wound- 
canal.  Gradually,  at  first  thinner,  later  thicker  layers  of  an 
inter-cellular  homogeneous  substance  are  formed,  and  the 
surrounding  lens-capsule  grows  thicker  by  the  new-formation 
of  vitreous  substance  on  its  inner  surface). 

Larger  wounds  of  the  lens-capsule  remain  permanently 
open,  and  this  is  due  to  the  folds  in  the  capsule  which  accord- 
ing to  Becker  are  observed,  or  to  the  rolling  up  of  the  lens- 
capsule,  as  Raab  and  myself  have  described.  This  rolling  up, 
as  stated  above,  takes  place  mostly  in  a  centrifugal,  sometimes 
in  a  centripetal  direction. 

In  consequence  of  these  larger  wounds  of  the  lens-capsule 
the  lens  substance  becomes  exposed  to  the  influence  of  the 
aqueous  humor  or  vitreous  body,  and  the  result  of  this 
exposure  is  the  formation  of  a  traumatic  cataract.  In  the 
simplest  form  of  these  cataracts,  we  find  the  lens  fibres  near 
the  capsular  wound  swollen  (by  imbibition)  and  granular. 
Gradually  these  lens  fibres  are  broken  up,  and  the  myeline 
becomes  free  and  can  be  absorbed.  The  capsular  epithelial 
cells  may  by  imbibition  swell  too,  and  appear  as  large  vesi- 
cle-like cells.  Becker  speaks  also  in  these  cases  of  an  inflam- 
matory new  formation  of  cells  and  "  giant-cells."  My  own 
examinations  have  not  enabled  me  to  agree  with  this  state- 
ment. 

In  this  way  the  whole  of  the  lens  substance  may  be  broken 
up  and  absorbed,  and  the  anterior  and  posterior  halves  of 


196 


THE  HUMAN  EYE. 


the  inner  surfaces  of  the  lens-capsule  may  become  adherent 
to  each  other. 

Ruptures  of  the  posterior  lens  capsule  cause  the  same 
conditions,  although  the  progress  seems  to  be  a  slower  one, 
and  we  frequently  then  find  particles  of  the  broken  lens  fibres 
suspended  in  the  vitreous  body. 

If,  in  consequence  of  the  injury,  the  iris  and  ciliary  body, 
or  the  whole  of  the  uveal  tract  become  inflamed,  the  conditions 
inside  the  ruptured  lens-capsule  may  appear  very  different. 
The  fibrino-plastic  exudation,  caused  by  these  inflammations, 
can  enter  the  wound  in  the  lens-capsule,  and  here  also  be 
transformed  into  connective-tissue,  which  gradually  leads  to 
destruction  of  the  lens  fibres.  The  new  formed  tissue  con- 
sisting of  round-cells  and  spindle-cells  lies  close  to  the  lens- 
capsule,  and  fills  all  its  folds  and  wrinkles.  Frequently  it  is 
seen   to  contain  new  formed  blood-vessels  which  are  some- 


FiG.  94.— Connective-tissue  within  the  ruptured  lens-capsule. 

times  of  comparatively  large  calibre.  (See  Fig.  94).  This 
tissue  is  exactly  the  same  which  Becker  has  described  as 
formed  within  the  intact  lens-capsule.  How  far  the  capsular 
epithelial  cells  help  to  form  this  tissue,  I  have  not  been  able 
to  ascertain,  as  they  were  always  wanting  in  my  specimens. 

I  once  found  the  same  tissue  inside  the  ruptured  capsule 
of  a  crystalline  lens,  which  had  been  dislocated  under  the 
conjunctiva. 

The  remainder  of  the  lens  fibres  in  these  cases  were 
always  granular  or  broken  up. 

This  new-formed  tissue  sometimes  glues  the  crystalline- 
lens  to  the  cornea,  and  probably  always  to  the  iris,  except 
where  it  is  found  in  dislocated  lenses,  and  the  conditions  are 
changed  accordingly.     Synechiae  between  the  usually  cata- 


LENS  CR  YSTALLINEA. 


197 


ractous  crystalline  lens  and  the  cornea  may,  as  we  have  seen, 
also  happen  when  the  capsule  is  perfectly  intact. 

The  osseous  tissue  sometimes  found  within  the  lens-cap- 
sule probably  always  takes  its  origin  from  such  new-formed 
connective-tissue.  Possibly  the  deposits  of  lime,  usually 
found  in  such  lenses,  have  a  direct  influence  upon  the  forma- 
tion of  osseous  tissue.  I  am  in  the  possession  of  an  eye  with 
general  ossification  of  the  choroid,  in  which  the  folded  lens- 
capsule,  which  lies  embedded  in  a  cyclitic  membrane,  is 
perfectly  filled  with  osseous  tissue.  The  origin  of  the  affec- 
tion was  an  injury.     (See  Fig.  95.)     I  have,  however,  not  yet 


Fig.  95. — Osseous-tissue  formed  within  the  ruptured  lens-capsule. 

seen  a  specimen,  where  the  whole  of  the  lens  substance  was 
changed  into  the  spindle  cell  tissue,  above  described. 

Foreign  bodies  are  sometimes  retained  in  the  lens  sub- 
stance. Iwanoff  states  that  they  are  then  found  to  be 
surrounded  with  pus  cells,  and  Becker  adds  that  these  pus 
cells  come  from  tissues  outside  the  lens-capsule. 


X. 

VITREOUS    BODY   AND   ZONULA   ZINNII. 

I.  Normal  Conditions  of  the   Vitreous  Body. 

The  vitreous  humour  consists  of  a  jelly-like  substance, 
in  which  cells  are  suspended. 

A  number  of  authors  are  of  the  opinion  that  the  vitreous 
body  is  inclosed  in  a  membrane,  the  so-called  membrana 
hyaloidea,  and  Schwalbe  has  recently  joined  in  this  view.  I 
cannot,  however,  agree  with  this  opinion.  According  to 
my  examinations,  no  such  limiting  membrane  belongs  to  the 
vitreous  body,  and  it  is  separated  from  the  retina  only  by  the 
limitans  interna  of  that  membrane.  The  jelly-like  substance 
of  the  vitreous  body  is,  however,  somewhat  tougher  and 
denser  in  its  periphery.  The  endothelial  and  epithelial  cells 
described  upon  the  membrana  hyaloidea,  I  am  convinced,  do 
not  exist. 

The  jelly-like  substance  consists  of  a  denser  mucoid  and 
a  thinner  fluid  part.  Most  authors  speak  of  concentric 
layers  in  the  denser  peripheral  part,  while  the  inner  part,  the 
nucleus,  is  said  to  be  more  homogeneous.  Schwalbe,  more- 
over, found  septa  in  the  vitreous  body  running  in  a  radiary 
direction,  and  one  septum  running  concentrically  with  the 
surface  of  the  vitreous  body.  After  having  hardened  the 
vitreous  body  in  a  dilute  solution  of  chromic  acid,  I  have  seen 
similar  conditions,  and  it  seems  therefore  that  we  have 
concentric  layers  in  the  periphery,  and  radius-like  septa 
between  which  the  thin  fluid  part  of  the  vitreous  body  is 
lying. 

A  canal  is  found  beginning  at  the  optic  papilla  and  run- 
ning through  the  vitreous  body  to  the  fossa  patellaris  (into 
which  latter  the  crystalline  lens  fits),  which  is  filled  with 
fluid,  the  so-called  canalis  hyaloideus.  During  foetal  life  this 
canal  encloses  the  arteria  hyaloidea.  By  injecting  a  stained 
fluid  into  the  intervaginal  space  of  the  optic  nerve,  this  canal 


VITREOUS  BODY  AND  ZONULA  ZINNIl.  jgg 

may  be  filled,  and  we  must  therefore  consider  it  to  be  a 
lymphatic  channel,  in  direct  communication  with  those  of  the 
optic  nerve  and  retina.  According  to  Schwalbe,  this  canal  is 
surrounded  by  a  vitreous  membrane  to  which  some  cells  are 
often  attached.  They  form,  however,  no  endothelial  coating 
of  this  canal,  but  are  the  cells  of  the  vitreous  body,  to  be 
spoken  of  directly. 

A  number  of  authors  have  found  fibrillae  in  the  vitreous 
body.  I  have  never  been  able  to  find  them  in  the  normal 
condition. 

The  vitreous  body  always,  however,  contains  cellular  ele- 
ments. They  appear  to  be  more  numerous  in  its  outer  than 
its  central  parts,  and  ScJnvalbe  calls  some  of  them  directly 
subhyaloid  cells.  The  same  cells  are,  however,  found  in  other 
parts  of  the  vitreous  body,  and  this  name  appears  therefore 
inappropriate. 

Iwanoff  makes  a  distinction  between  three  separate  kinds 
of  cells  in  the  vitreous  body.  Although  they  may  be  here 
referred  to  as  different  types,  I  must  state  that  these  cells  are 
very  variable  in  shape,  and  the  different  kinds  are  seen  to 
merge  into  each  other.  We  find  round-cells  with  one  or  more 
nuclei,  some  of  which  are  seen  to  contain  smaller  and  larger 
vacuolae,  by  which  the  nucleus  is  crowded  to  one  side,  and 
which  appear  like  seal  rings.  Then  we  find  cells  with  one  or 
more  offsets,  and  of  an  accordingly  varying  aspect.  The 
third  kind  of  cells  described  by  Iwano^  contain  light  vesicles, 
which  are  said  to  be  filled  with  a  fluid,  and  are  perhaps, 
identical  with  those  containing  vacuolae.  Liebcr  and  Ktiehn 
saw  minute  granules  taken  up  by  these  cells,  in  molecular 
motion.  These  cells,  furthermore,  have  been  considered  as 
producing  the  mucoid  tissue  of  the  vitreous  body,  and  have 
accordingly  been  called  physaliphora. 

With  regard  to  the  nature  of  all  these  cell  forms,  I  must 
agree  with  Schwalbe,  who  declares  them  to  be  lymph  cells, 
that  is,  wandering  cells  coming  from  the  membranes  sur- 
rounding the  vitreous  body. 

2.  Pathological  Conditions. 
The  question  whether  the  vitreous  body  can  become  in- 


200  ^^^  HUMAN  E  YE. 

flamed,  independent  of  an  inflammatory  process  in  any  of 
the  surrounding  membranes,  has  of  late  been  frequently 
discussed.  Since  the  vitreous  body  has  neither  blood-vessels 
nor  cells  of  its  own,  we  are  justified,  it  seems,  in  denying  a 
priori,  the  possibility  of  such  an  independent  inflammation. 
Experiments  made  in  order  to  solve  the  question,  have  led 
to  the  same  result,  since  it  is  simply  impossible  to  bring  a 
foreign  substance  into  the  vitreous  body  with  the  intention 
of  there  creating  an  inflammation,  without  piercing  other  mem- 
branes of  the  eye  ball,  which  can  thus  become  inflamed.  The 
best  conditions  for  such  experiments  would  be  found  in  an 
eye,  from  which  the  crystalline  lens  had  been  removed,  while 
the  posterior  lens-capsule  remained  intact,  by  bringing  the 
foreign  substance  into  the  eye  ball  through  cornea  and  lens- 
capsule.  Schmitt-Rimpler  has  used  such  eyes  for  his  experi- 
ments. But  even  in  these  eyes  the  hyalitis,  caused  by  the 
experiment,  does  not  prove  the  possibility  of  an  independent 
inflammation  of  the  vitreous  body.  Pagenstecher  has,  further- 
more, directly  observed  by  experiments,  that  the  cells  found 
in  the  vitreous  body  thus  artificially  irritated,  come  from  the 
surrounding  membranes. 

I  agree  therefore  with  those  authors,  who  deny  the  possibil- 
ity of  an  independent  inflammation  of  the  vitreous  body,  and 
can  only  acknowledge  the  existence  of  secondary  hyalitis.  As 
we  find  in  the  contents  of  the  synovia  of  a  joint  the  results  of 
a  serous,  fibrinous  or  purulent  inflammation  of  this  membrane, 
so  we  find  in  the  vitreous  body  the  products  of  the  inflam- 
matory processes  of  the  surrounding  membranes.  These 
latter  may,  hov^^ever,  show  a  different  form  of  inflammation 
from  the  one  found  in  the  vitreous  body,  as  the  cells  when 
once  exuded  into  the  latter  have  ample  space  for  further 
changes. 

A,  Liquefaction  of  the   Vitreous  Body  {Sync hisis). 

Chronic  affections  of  the  uveal  tract  may  produce  a  change 
in  the  consistency  of  the  vitreous  body,  which  finally  leads  to 
its  complete  liquefaction. 

Von  Wccker  states  that  this  liquefaction  is  caused  by  a 
large    number  of  cells   which   immigrate    into    the  vitreous 


VITREOUS  BODY  AND  ZONULA  ZINNII.  20I 

body.  This  appears,  however,  not  to  be  the  case,  as  the 
immense  number  of  cells  found  in  the  vitreous  body  in  a 
case  of  purulent  hyalitis  do  not  cause  synchisis.  Moreover, 
he  explains  the  opacities,  clinically  observed  in  such  a  lique- 
fied vitreous  body,  by  these  cells. 

We  sometimes  find  in  the  liquefied  vitreous  crystals  of 
cholesterine,  and  then  the  disease  is  clinically  styled  synechisis 
scintillans.  Recently  Poncet  also  found  crystals  of  tyrosine 
and  phosphates  in  a  case  of  synchisis  scintillans. 

B.  Plastic  Hyalitis, 

When  describing  the  conditions  which  exist  during  the 
inflammation  of  the  ciliary  body  and  especially  the  formation 
of  cyclitic  membranes,  we  had  to  mention  plastic  hyalitis  in 
the  fossa  patellaris  which  helps  considerably  in  the  formation 
of  these  structures. 

We  jind  at  first  a  larger  number  of  round-cells  immigrating 
into  the  vitreous  body  which  then  appear  to  lie  chiefly  behind 
the  lens,  often  embedded  in  a  fibrinous  coagulum,  which  grad- 
ually go  over  into  spindle-cells  and  lead  to  the  formation  of 
a  tough  connective-tissue  with  new-formed  blood-vessels. 

The  same  process  is  observed,  if  a  foreign  body  has 
pierced  the  vitreous.  The  immigrated  cells  then  chiefly 
lie  along  the  wound  canal,  and  again  are  transformed  into 
connective-tissue.  I  possess  a  specim.en  of  an  eye,  injured  by 
a  piece  of  a  gun  cap  which  perforated  the  cornea,  iris,  lens  and 
vitreous  body  before  becoming  retained  in  the  sclerotic, 
choroid  and  retina  at  the  opposite  side  of  the  eye  ball.  In 
spite  of  the  ensuing  purulent  iritis  and  cyclitis,  the  inflamma- 
tion in  the  vitreous  body  remained  confined  to  the  wound 
canal,  and  led  to  the  formation  of  a  band  of  tough  connective- 
tissue  running  from  the  place  of  its  entrance  to  the  place 
where  the  foreign  body  became  embedded  in  the  sclerotic. 

Such  a  new-formation  of  connective-tisspe  in  the  vitreous 
body  is  also  seen  after  haemorrhages  into  its  structure.  We 
then  generally  find  a  small  amount  of  fibrine  filled  with  round- 
cells  and  surrounded  by  the  red  blood-corpuscles.  Gradually 
this  fibrine  is  changed  into  connective-tissue,  in  the  formation 


202  THE  HUMAN  EYE. 

of  which  the  red  blood-corpuscles  also  seem  to  take  an  active 
part  as  they  entirely  disappear. 

We  had,  furthermore,  occasion  to  mention  plastic  hya- 
litis,  occasioned  by  affections  of  the  retina  and  optic  nerve.  I 
mean  here  the  new-formation  of  connective-tissue  in  the 
excavated  optic  papilla,  and  the  membrane  like  new-formations 
upon  the  inner  surface  of  the  inflamed  retina.  In  these  cases 
the  plastic  hyalitis  only  concerns  the  outer  layers  of  the 
vitreous  body. 

If  such  membranous  new-formations  do  not  adhere  to  the 
retina,  they  may  by  their  retraction  lead  to  detachment 
of  the  vitreous  body,  in  which  the  substance  of  the  latter 
becomes  naturally  condensed.  We  find  this  detachment,  as 
has  first  been  made  known  by  Iwanoff,  in  a  number  of 
pathological,  especially  injured  eye  balls,  and  most  frequently 
when  a  foreign  body  has  become  encapsuled  in  the  vitreous. 

Von  Wecker  mentions  an  observation  made  by  Poncet, 
which  proves  that  the  connective-tissue  in  the  posterior  parts 
of  the  vitreous  body  too,  can  be  ossified.  The  formation 
of  osseous  tissue  in  cyclitic  membranes  has  been  mentioned 
above. 

The  blood-vessels  found  in  the  connective-tissue  which  is 
formed  in  the  vitreous  body,  come  from  the  ciliary  body,  the 
retina  or  the  optic  nerve. 

The  vitreous  body  may  also  become  detached  by  fluids 
which  are  found  to  lie  between  it  and  the  retina,  and  this 
mode  of  detachment  seems  to  be  caused  more  by  chemical 
than  by  mechanical  influences.  If  this  were  not  the  case,  the 
fluid  would  certainly  be  taken  up  by  the  vitreous  body,  and 
the  detachment  thus  heal. 

C.  Purulent  Hyalitis. 

After  injuries,  and  in  the  course  of  a  purulent  inflamma- 
tion of  the  uveal  tract  or  during  purulent  panophthalmitis 
we  may  find  purulent  hyalitis,  which  is  characterized  by  the 
presence  of  an  immense  number  of  cells  in  the  vitreous  body. 
Their  number  may  be  so  large  that  it  is  hardly  possible  to  see 
anything  but  cells.     The  latter  have  all  sorts  of  shapes,  and 


VITREOUS  BODY  AND  ZONULA  ZINNII.  203 

frequently  two  or  more  nuclei.  They  have  sometimes  very 
long  thin  offsets,  which  appear  like  a  network  of  fibrillae. 

This  condition  may  lead  to  perforation  of  the  eye  ball  or 
it  may  become  chronic  and  lead  to  the  formation  of  connec- 
tive-tissue, which  is  one  of  the  chief  factors  from  which  the 
shrinking  of  the  eye  ball,  clinically  called  phthisis  bulbi 
results. 

In  rare  cases  this  formation  of  connective-tissue  is  very 
quickly  accomplished,  and  concerns  the  whole  of  the  vitreous 
body  and  may  lead  to  the  incorrect  diagnosis  of  introcular 
tumor.  It  may  furthermore  make  the  eye  ball  as  hard  as  in 
glaucoma,  and  when  shrinking  produce  again  phthisis  bulbi. 

Anatomically  we  can  speak  of  phthisis  bulbi  only,  when  the 
vitreous  body  has  thus  been  changed,  and  we  must  make  a 
more  distinct  separation  between  anterior  phthisis  and 
phthisis  bulbi,  than  this  is  usually  done  by  clinicists. 

The  Zonula  Zinnii. 

I.  Normal  Conditions. 

In  the  region  of  the  ora  serrata,  a  number  of  well  con- 
toured, light  and  tough  fibres  are  seen  to  spring  from  the 
vitreous  body,  of  which  they  are  a  part,  as  J.  Arnold  has 
proven.  They  lie  at  first  upon  the  retinal  layer  of  the  ciliary 
body,  and  follow  all  its  windings  up  to  the  most  anterior 
portion  of  that  body.  From  there  they  are  bent  inward  and 
pass  on  to  the  anterior  and  posterior  lens-capsule  ;  some  of 
them  return  to  the  vitreous  body.  They  have  therefore  like 
the  ciliary  body  a  pars  plicata  and  a  pars  non-plicata.  These 
fibres  which  hold  the  crystalline-lens  in  position  are  called 
zonula  zinnii  (ligamentum  suspensorium  lentis,  zonula  ciliaris). 
They  are  arranged  in  bundles  by  a  very  fine  and  easily  de- 
stroyed homogeneous  substance,  after  they  have  bent  inward 
from  the  ciliary  body.  According  to  J.  Arnold,  we  find  be- 
sides these  fibres,  which  run  in  a  meridional  direction,  a  num- 
ber which  after  having  run  a  short  time  in  this  direction,  go 
over  into  an  equatorial  one. 

Some  authors  have  seen  a  transverse  striation  on  these 
fibres,  and  therefore  considered  them  to  be  of  a  character  mus- 


204  THE  HUMAN  EYE. 

cular  Cells  sometimes  found  between  them,  are  wandering 
(lymphatic)  cells. 

Where  the  zonula  fibres  are  merged  into  the  lens-capsule, 
this  latter  appears  thickened. 

2.  Pathological  Conditions. 

Pathological  changes  in  the  tissue  of  the  vitreous  body 
must  needs  influence  the  condition  of  the  fibres  of  the  zonula 
Zinnii.  There  have,  however,  but  few  pathological  changes 
of  these  fibres  been  observed.  Becker  states  that  they  may 
become  thin  and  atrophic,  or  thickened  and  granular. 

When  the  fibres  of  the  zonula  have  been  severed,  they 
appear  wavy  like  elastic  fibres. 


THE  END. 


1 1^  D  E  X. 


Abscess  of  the  cornea,  i6. 

Arachnoidal  sheath  of  the  optic  nerve, 

142. 
A  reus  senilis  cornea,  39. 
Argyrosis  conjunctival,  63. 
Atrophy  of  choroid,  134. 
iris, 92, 

lens  capsule,  190. 
optic  nerve,  153. 
retina,  187. 
Bowman's  layer,  2. 

Bruch's  membrane,  83. 
Burns  with  lime  of  conjunctiva,  64. 
of  cornea,  37. 
Canalis  hyaloideus. 
Capsule  of  lens,  187. 
Capsular  epithelium  of  lens,  188. 
Cataracta,  190. 

hemorrhagic,  194, 
nigra,  191. 
polar  anterior,  193. 
pyramidal,  193. 
soft,  [92. 
traumatic,  194. 
Choroidea,  116. 

atrophy  of,  134. 
blood-vessels  of,  116. 
cystoid  formations  in,  138. 
granuloma  of,  138. 
nerves  of,  117. 
ossification,  135. 
pigmented  epithelium,  119. 
sarcoma  of,  138. 
tubercles  of,  131. 
Choroiditis,  135. 
Choroiditis  atrophic,  127. 

disseminate,  130. 
exudative  areolar,  130. 
parenchymatous,  130. 
plastic,  127. 
purulent,  130. 
serous,  135. 
Chorio-retinitis  centralis,  130. 

disseminate,  130. 
Ciliary  staphyloma,  48. 
Circulus  iridis  major,  82. 
minor,  82. 
Cone-fibres  of  retina,  164. 
Conjunctiva  bulbi,  55. 


blood-vessels  of,  57. 
inflammation  of,  58. 
injuries  to,  63. 
lymph-vessels  of,  57. 
nerves  of,  57. 
tumors  of,  65. 
Conjunctival  oedema,  57. 

haemorrhage,  57. 
Conjunctivitis,  58. 

blennorrhoic,  59. 
catarrhal,  58. 
croupous,  61. 
diptheritic,  61. 
gonorrhoic,  57. 
phlyctsenular,  58. 
purulent,  59. 
trachomatous,  61. 
Cornea,  i. 

abscess  of,  16. 
blood-vessels  of,  10. 
cysts  of,  35. 
fistule  of,  34. 
infiltration  of,  11. 
inflammation  of,  13. 
injuries  to,  31. 
lymphatic  canals  of,  3. 
necrosis  of,  32. 
nerves  of,  10. 
ossification  of,  24. 
scars  of,  23. 
ectatic  of,  35. 
sclerosis  of,  16. 
synechiae  with  iris,  25. 
lens,  37. 

vitreous  body,  37. 
tumors  of,  38. 
ulcer  of,  19. 
xerosis  of,  39. 
Cornea-scleral  margin,  8. 

staphyloma,  47. 
Corpus  ciliare,  99. 

atrophy  of,  113. 
blood-vessels  of,  loi. 
gumma  of,  no. 
hypertrophy  of,  113. 
injuries  to,  113. 
muscles  of,  99. 
nerves  of,  loi. 
retinal  layer  of,  103. 


2o6 


INDEX. 


rupture  of,  114. 
tumors  of,  115. 
uveal  layer  of,  103. 
Cyclitic  membranes,  iii. 
Dermoid  Tumors,  see  tumors. 
Descemet's  membrane,  6. 
Detachment  of  ciliary  body,  112. 
retina,  179. 
vitreous  body,  143. 
Dislocation  of  lens  under  conjunctiva  64. 
Dura  mater  sheath  of  optic  nerve,  142. 
Episcleral  tissue,  56. 
Episcleritis,  58. 
Epithelioma,  see  tumors 
Excavation  of  optic  papilla,  155. 
Fibrinous  choroiditis,  127. 
iritis,  87. 
Fibromatous  tumors,  see  tumors. 
Fontona's  spaces,  9. 
Foreign  bodies  in  choroid,  136. 

conjunctiva,  64. 
cornea,  31. 
corpus  ciliare,  113. 
iris, 93. 
lens.  197. 
retina,  i8j. 
sclerotic,  53. 
vitreous  body,  301. 
Fovea  centralis,  167. 
Glaucoma,  155. 

Glaucomatous  excavation  ofpapilla,  155 
Granulomata,  see  tumors. 
Haller's  vascular  ring,  146 

Haemorrhage  in  choroid,  136. 

conjunctiva,  57. 
iris,  86. 

optic  nerve,  156. 
retina,  178. 
vitreous  body,  201 
Haemorrhagic  cataract,  194. 
Hyalitis,  201. 

plastic,  201. 
purulent,  202. 
Hyaloid  artery,  198. 
canal,  198. 
Hypopyon,  17. 
iDflammation  of  choroid,  135. 

ciliary  body,  103. 
conjunctiva,  58. 
cornea,  n. 
iris,  84. 

optic  nerve,  150. 
retina,  169. 
sclerotic,  43. 
vitreous  body,  301. 
Injuries  to  choroid,  136. 

ciliary  body,  113. 
conjunctiva,  61. 


cornea,  31. 

iris,  93. 
lens,  194. 
optic  nerve,  157. 
retina,  183. 
sclerotic,  53. 
Interfascicular  canals,  4. 
Interfibrillar  canals,  3. 
Interlamellar  canals,  4. 
Interstitial  neuritis,  150. 
retinitis,  174. 
Intervaginal  space,  144. 
Iris,  81. 

atrophy  of,  92. 
blood-vessels  of,  83. 
cysts  of,  94. 
endothelium  of,  81. 
incatceration  ot,  37. 
injuries  to,  93. 
muscles  of,  83. 
nerves  of,  S3, 
prolapse  of,  39. 
synechiae  anteriores  of,  36. 

posteriores  of,  91. 
uveal  layer,  83. 
Iritis,  84. 

fibrinous,  87. 
haemorrhagic,  86. 
parenchymatous,  89. 
plastic,  87. 
purulent,  89. 
serous,  84. 
Keratitis,  11. 

parenchymatous,  15. 
phyctaenular,  15. 
purulent,  16. 
striped,  15. 
Keratoconus,  39. 
Keratomalacia,  32. 
Lamina  cribrosa,  40. 
fusca,  103. 

vitrea  choroideae,  ii8. 
Lens,  1S7. 
Lens-capsule,  187. 

epithelium,  18S. 
fibres,  188. 
Leucosarcoma,  see  tumors 
Ligamentum  pectinatum,  9. 
Limitans  externa,  161. 
Limitans   interna,  160. 
Lipomatous  tumors,  see  tumors. 
Lymphangiectasia,  65. 
Macula  lutea,  167. 

Medullary  neuritis,  153. 
Melanocancroid  tumors,  see  tumors. 
Melanoma,  see  tumors. 
Melanosarcoma,  see  tumors. 


INDEX. 


207 


Myocephalon,  32. 
Nervi  ciliares  breves,  117. 
longi,  117. 
Nervous  opticus,  142. 

blood-vessels  of,  146. 
sheaths  of,  142. 
Neuritis,  150. 

interstitial,  150. 
medullary,  152. 
Neuro- epithelial  layer  of  retina,  163. 
Normal  conditions  of  choroid,  ti6. 
ciliary  body,  yg. 
conjunctiva,  55. 
cornea,  i. 
iris,  81. 
lens,  187. 
optic  nerve,  i42. 
retina,  159. 
sclerotic,  39. 
vitreous  body,  198, 
zonula  zinnii,  203, 
CEdema  of  conjunctiva,  57. 
optic  nerve,  147. 
retina,  16S. 
Opticus,  142. 

Ora  serrata  of  retina,  165. 
Ossification  of  choroid,  132. 

choroidal  sarcoma,  141. 
cornea,  24. 
vitreous  body,  loi. 
Osteoma,  see  tumors. 
Pannus.,  23. 

Papillioraa,  see  tumors, 
Pathological  conditions  of  choroid,  120. 
ciliary  body,  103, 
conjunctiva,  58. 
cornea,  11. 
iris,  84. 
lens,  190. 
optic  nerve,  146. 
retina,  168. 
sclerotic,  43. 
vitreous  body,  199 
zonula  zinnii,  204. 
Phlyctenula  of  conjunctiva,  59. 

cornea,  15. 
Phthisis  anterior,  24. 

bulbi  totalis,  203. 
Physaliphora,  199. 
Pia  mater  sheath,  143. 
Pigmented  cells  of  choroid,  116. 
cornea,  6. 
iris,  82. 
sclerotic,  39. 
Pigmented  epithelium,  119. 
Pinguecula,  56. 
Polypoid  tumors,  see  tumors. 


Prolapse  of  iris,  36. 
Pterygium,  30. 
Pupillary,  membrane,  88. 
Recklinghausen's  canals,  3. 
Reichert's  layer,  a. 
Results  of  choroiditis,  133. 
cyclitis,  III. 
iritis,  91. 
keratitis,  33. 
neuritis  optica,  153. 
retinitis,  180. 
scleritis,  44. 
Retina,  159. 

ciliary  part  of,  103. 
detachment  of,  112, 
external  limiting  membrane  of,  161. 
ganglionic  layer  of,  161. 
inner  granular  layer  of,  162. 
inner  molecular  layer  of,  163. 
internal  limiting  membrane  of,  160. 
nerve  fibre  layer  of,  i6i. 
outer  granular  layer  of,  163. 
outer  molecular  of,  163. 
rods  and  cones,  163. 
tumors  of,  183. 
Retinitis,  169. 

albuminuric,  169. 
apoplectic,  179. 
atrophic,  174. 
pigmentary,  133. 
purulent,  177. 
Rod-fibres,  163. 
Rod-granules,  164. 
Sarcomatous  tumors,  see  tumors 
Schlemm's  canal.  41. 
Scleral  staphyloma,  47. 
ciliary,  48. 
equatorial,  49. 
posterior,  49. 
partial,  47. 
total,  47. 
Scleritis,  42. 

infiltration,  42. 
purulent,  43. 
Sclerotic,  39- 

atrophy  of,  46. 
blood-vessels  of,  41. 
ectasy  of,  46. 
hypertrophy  of,  45. 
nerves  of,  41. 
scars  of,  44. 
tumors  of,  54. 
Serous  cysts,  see  tumors. 
Subarachnoidal  space,  144. 
Subhyaloid  cells,  199. 
Subvaginal  space,  144. 
Synchisis  simplex,  300. 
scintillans,  301. 


2o8 


INDEX. 


Trachoma,  6i. 

Tumors  of  the  choroid,  138. 

cysts,  138. 

enchondroma,  139. 

granuloma,  138. 

sarcoma,  138. 
Tumors  of  the  ciliary  body,  115. 

myoma,  115. 

sarcoma,  115. 

Tumors  of  the  conjunctiva,  65. 

cysts,  serous,  65. 

dermoid  tumors,  67. 

epithelioma,  74. 

fibroma,  69. 

granuloma,  td. 

leucosarcoma,  71. 

lipoma,  67. 

lymphangiectasia,  65. 

melanocancroid  tumors, 

melanosarcoma,  71. 

osteoma,  69. 

papilloma,  69. 

polypoid  tumors,  66. 
Tumors  of  the  cornea,  38. 
Tumors  of  the  iris,  97. 


cysts,  94. 

epidermoidoma,  9$. 
granuloma  traumaticum,  97- 
leucosarcoma,  98. 
melanoma,  97. 
melanosarcoma,  98. 
Tumor  of  the  optic  papilla,  157. 
Tumors  of  the  retina,  182. 
fibroma,  183. 
glioma,  182. 
sarcoma,  182. 
Tumors  of  the  sclerotic,  54. 
Ulcer  of  the  cornea,  19. 
Vaginitis  nervi  optic,  149. 
Venae  vorticosse,  117. 
Viterous  body,  198. 

detachment  of,  133. 
inflammation  of,  igg. 
liquefaction  of,  200. 
synechia  with  cornea,  27. 
Vitreous  bodies  of  the  lamina   vitrea 
choroidese,  121. 
Xerosis  of  conjunctiva,  63. 

cornea,  39. 
Zonula  of  Zinn,  203. 


UNIVERSITY  OF  CALIFORNIA  UBRARY 

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This  book  is  DUE  on  the  last  date  stamped  below. 


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